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Books on the topic 'Kidney cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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1

Glomerulopathies: Cell biology and immunology. Australia: Harwood Academic Press, 1996.

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2

International, Meeting on Anion Transport Protein of the Red Blood Cell Membrane as well as Kidney and Diverse Cells (1989 Fukuoka-shi Japan). Anion transport protein of the red blood cell membrane: Proceedings of the International Meeting on Anion Transport Protein of the Red Blood Cell Membrane as well as Kidney and Diverse Cells, Fukuoka, 1-3 May 1989. Amsterdam: Elsevier, 1989.

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3

Edson, Pontes J., and Bukowski Ronald M, eds. Clinical management of renal cell cancer. Chicago: Year Book Medical Publishers, 1990.

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4

L, Minetti, D'Amico G. 1929-, and Ponticelli C, eds. The Kidney in plasma cell dyscrasias. Dordrecht: Kluwer Academic Publishers, 1988.

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5

Minetti, Luigi, Giuseppe D’Amico, and Claudio Ponticelli, eds. The Kidney in Plasma Cell Dyscrasias. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1315-8.

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6

Debruyne, F. M. J., 1941- and Ackermann R. 1941-, eds. Immunotherapy of renal cell carcinoma: Clinical and experimental developments. Berlin: Springer-Verlag, 1991.

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7

Lara, Primo N., and Eric Jonasch. Kidney cancer: Principles and practice. Heidelberg: Springer-Verlag, 2012.

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8

C, Bollack, Jacqmin D, and European Organization for Research on Treatment of Cancer. Genito-Urinary Tract Cancer Cooperative Group., eds. Basic research and treatment of renal cell carcinoma metastasis: Proceedings of an EORTC Genitourinary Group meeting, held in Strasbourg, France, November 4, 1988. New York: Wiley-Liss, 1990.

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9

Renal cell carcinoma. Shelton, Conn: People's Medical Pub. House, 2009.

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10

International Subcellular Methodology Forum (10th 1986 University of Surrey). Cells, membranes, and disease, including renal. New York: Plenum Press, 1987.

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11

H, Bach P., Lock E. A, and Mudge Gilbert H, eds. Renal heterogeneity and target cell toxicity: Proceedings of the Second International Symposium on Nephrotoxicity, University of Surrey, UK, 6-9 August 1984. Chichester: Wiley, 1985.

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12

service), SpringerLink (Online, ed. Acquired Cystic Disease of the Kidney and Renal Cell Carcinoma: Complications of Long-Term Dialysis. Tokyo: Springer, 2007.

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13

Amato, Robert J. Emerging research and treatments in renal cell carcinoma. Rijeka: InTech, 2012.

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14

Hikaru, Koide, Endou Hitoshi, and Kurokawa Kiyoshi, eds. Cellular and molecular biology of the kidney: Int. Symposium on Cell Biology of Nephron Heterogeneity--Fine Structure and Functions, Shizuoka, July 22-25, 1990. Basel: Karger, 1991.

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15

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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16

H, Kinne Rolf K., ed. Renal biochemistry: Cells, membranes, molecules. Amsterdam: Elsevier, 1985.

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17

Kidney Cancer (Cancer Treatment and Research). Springer, 2003.

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18

Chang, T. Artificial Kidney, Artificial Liver, and Artificial Cells. Springer, 2013.

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19

Chang, T. Artificial Kidney, Artificial Liver, and Artificial Cells. Springer London, Limited, 2012.

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20

Chang, T. Artificial Kidney, Artificial Liver, and Artificial Cells. Springer, 2013.

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21

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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22

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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23

Winyard, Paul. Human kidney development. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0343.

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The kidneys perform diverse functions including excretion of nitrogenous waste products, homeostasis of water, electrolytes and acid–base balance, and hormone secretion. The simplest functional unit within the kidneys is the nephron, which consists of specialized segments from glomerulus, through proximal tubule, loop of Henle, and distal tubule. Human nephrogenesis starts with two stages of transient kidneys, termed the pronephros and mesonephros, and ends with development of a permanent organ from the metanephros on each side. The latter consists of just a few hundred cells when it is formed in the fifth week of pregnancy but progresses to a nephron endowment of between 0.6 to 1.3 million by the time nephrogenesis is completed at 32–36 weeks of gestation. Key events during this process include outgrowth of the epithelial ureteric bud from the mesonephric duct, interactions between the bud and the metanephric blastema (a specific region of mesenchyme) that cause the bud to branch and mesenchyme to condense, epithelialization of the mesenchyme to form proximal parts of the nephron, and differentiation of segment specific cells. Molecular control of these events is being unpicked with data from human genetic syndromes and animal models, and this chapter highlights several of the most important factors/systems involved. Increased understanding of development is not just relevant to congenital kidney malformations, but may also be important in designing rational therapies for diseases of the mature kidney where recapitulation of developmental pathways is common.
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24

Drugs and kidney. New York: Raven Press, 1986.

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25

University, Pennsylvania State, and United States. National Aeronautics and Space Administration., eds. Kidney cell electrophoresis: Comprehensive final progress report. University Park, Pa: Pennsylvania State University, 1985.

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26

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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27

Stewart, Douglas, Gaurav Shah, Jeremiah R. Brown, and Peter A. McCullough. Contrast-induced acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0246.

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Contrast-induced acute kidney injury (CI-AKI) occurs because all forms of intravascular contrast contain iodine and their biochemical structures induce immediate changes in systemic and renal vasoreactivity. In the kidneys, contrast induces a transient decrease in renal blood flow. This is more pronounced in patients with chronic kidney disease and diabetes mellitus. The reduction in blood flow allows slowed transit of contrast and reabsorption by the proximal tubular cells where contrast is directly toxic resulting in tubular cell dysfunction and death. When there is considerable damage, a transient rise in serum creatinine and reduction in urine output will be observed in the hours to days after contrast exposure. Principles to reduce CI-AKI include limiting the amount of contrast used, intravascular volume expansion to maximize renal blood flow and speed transit of contrast, and possibly agents to reduce the oxidative damage caused by the contrast agents themselves.
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28

Pollard, Hilary Jane. Studies on the localisation of eukaryotic initiation factors in Xenopus kidney B3.2 cells. 2002.

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29

Renal Cell Carcinoma. Oxford University Press, 2014.

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30

Jin, Ken *. The study of the effects of the quinolone antibiotics on mammalian cells with reference to ciprofloxacin and monkey kidney cells. 1989.

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31

Turner, Neil. Mechanisms of progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0136.

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Three major hypotheses attempt to explain progressive kidney disease following diverse diseases and injuries. To varying degrees they can explain the observed risk factors for progression and the ability of interventions to lower risk. The hyperfiltration hypothesis argues that progression is due to stress on residual nephrons leading to injury and damage to remaining glomeruli. The toxicity of proteinuria hypothesis proposes that serum proteins or bound substances are toxic to tubular or tubulointerstitial cells. This sets up cycles of damage which lead to tubulointerstitial scarring. The podocyte loss hypothesis contends that proteinuria is simply a biomarker for damaged or dying podocytes, and that it is further podocyte loss that leads to progressive glomerulosclerosis. Renoprotective strategies might have direct effects on podocytes. Importantly these different hypotheses suggest different therapeutic approaches to protecting the function of damaged kidneys. Differences between repair mechanisms may explain why some injuries lead to recovery and others to progressive disease, and may suggest new targets for protective therapy.
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32

Vaziri, Nosratola D. Oxidative stress and its implications in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0112.

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Reactive oxygen species (ROS) are produced at low levels physiologically and their production conveys signals and has specific functions. Control mechanisms ensure that this does not cause damage. ROS are highly reactive and cytotoxic and are also deliberately produced by inflammatory cells (granulocytes, macrophages) to kill pathogens. If these chemicals are released inappropriately or excessively, or if control mechanisms are under-functioning, bystander or unintended tissue damage may be caused. The concept of oxidative stress is based on the idea that in certain states, commonly inflammatory states, release of oxygen radicals may be excessive, or control mechanisms weakened, so that tissue damage occurs. In CKD, both overproduction and diminished control may apply. No effective therapies acting via these pathways have been established so far though there remain some candidates.
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33

Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0139.

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Experimental studies show that podocyte death first causes focal scars, but beyond approximately 40% loss is lethal to a glomerulus. Podocytes have limited ability to regenerate, although some degree of replacement may occur from stem cells located near the urinary pole of Bowman’s capsule. It is not yet known whether this plays a significant part in ameliorating damage in disease processes. In one interpretation, foot process effacement may be seen as an adaptation by the podocyte to remain attached to the glomerular basement membrane after injury, at the expense of proteinuria. Podocyte dysfunction is closely associated with proteinuria, which in turn is strongly associated with progressive loss of glomerular filtration rate. Continuing podocyte damage and loss could therefore account for progressive renal disease. In this hypothesis, drugs that protect against progression of renal disease may have their primary protective effects on podocytes themselves, rather than or as well as on haemodynamic factors or on fibrotic processes.
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34

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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35

Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.

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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.
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36

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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37

Mutter, Walter P. Urinalysis. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0006.

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Physicians have examined urine for over 6000 years. Urine microscopy was first employed to diagnose kidney disease in the seventeenth century and remains an indispensable tool. The value of urinalysis for diagnosis and management of renal and genitourinary disease is well accepted. Urinalysis aids in the diagnosis of renal disease especially in cases when a renal biopsy is not immediately available or is contraindicated. It is most informative when done by the treating physician with knowledge of the clinical context. Inspection is done by eye. Routine chemical analysis is done by dipstick but urine microscopy is essential for it may reveal abnormalities even when chemical evaluation is normal. Dysmorphic red cells, red cell casts, white blood cells, renal cells, and specific crystals may be diagnostically important. Urinalysis and microscopy can narrow the differential diagnosis faster than many more complex tests are able to.
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38

Connor, Thomas, and Patrick H. Maxwell. Hypoxia-inducible factor and renal disorders. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0331.

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Hypoxia-inducible factors (HIFs) are transcription factors that control the cellular response to changes in oxygen levels. This response is common to all cells in the body and is highly conserved in evolution. The kidney exhibits steep gradients in oxygenation which are important in the homeostatic response to anaemia. The cellular response to low levels of oxygen (hypoxia) also plays a role in such diverse processes as acute kidney injury, the progression of chronic kidney disease, and kidney cancer. There is now considerable interest in using drugs to manipulate the HIF response to treat these varied conditions.
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39

Douglas, Kenneth. Bioprinting. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190943547.001.0001.

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Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will learn about bioink—a bioprinting material containing living cells and supportive biomaterials. In addition, readers will become at ease with concepts such as fugitive inks (sacrificial inks used to make channels for blood flow), extracellular matrices (the biological environment surrounding cells), decellularization (the process of isolating cells from their native environment), hydrogels (water-based substances that can substitute for the extracellular matrix), rheology (the flow properties of a bioink), and bioreactors (containers to provide the environment cells need to thrive and multiply). Further vocabulary that will become familiar includes diffusion (passive movement of oxygen and nutrients from regions of high concentration to regions of low concentration), stem cells (cells with the potential to develop into different bodily cell types), progenitor cells (early descendants of stem cells), gene expression (the process by which proteins develop from instructions in our DNA), and growth factors (substances—often proteins—that stimulate cell growth, proliferation, and differentiation). The book contains an extensive glossary for quick reference.
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40

Mclver, Bryan, Peter J. Tebben, and Pankaj Shah. Endocrinology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0200.

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Numerous chemical messages control various functions at the levels of cells, organs, and organ systems. Such messages may be autocrine (the chemical message directly affects the cell producing it), paracrine (the message has local effects), or endocrine (the message has distant sites of action). Typically, endocrine effects are caused by hormones that are produced by specialized organs, although several important endocrine functions are performed by nonglandular tissues, most prominently the liver and the kidney. Disorders of the hypothalamus, ovaries, testes, and pituitary, thyroid, and adrenal glands are reviewed.
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41

Turner, Neil. Exercise-related pseudonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0049.

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Vigorous and prolonged physical exercise can produce a range of urinary abnormalities which would normally be considered alarming. They include haematuria, haemoglobinuria, the appearance in urine of red cells in urine, some fragmented in a ‘glomerular’ manner, red cell cast formation, and proteinuria. A variety of names have been given to these syndromes, including march haematuria and march haemoglobinuria. Mostly these changes seem benign and self-limiting. Rarely they are associated with acute kidney injury but this is often in the context of other renal insults, extreme dehydration, or hyperpyrexic conditions. Vigorous exercise is also commonly associated with various electrolyte changes related to both over- and under-hydration. These can complicate assessment. Transient proteinuria in the absence of haematuria appears to be a physiological response to even short-term exercise, its degree related to the intensity of the exercise. Causation of these syndromes is mixed and not fully explained. There is good evidence for physical trauma to red cells being a significant part, but this cannot explain the appearance of glomerular red cells and red cell casts. Exercise-related changes mostly resolve within less than a day, and almost all by 72 hours.
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42

Clinical transplants 2002. Los Angeles: UCLA Immunogenetics Center, 2002.

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43

Duffield, Jeremy S. Disordered scarring and failure of repair. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0140.

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Scarring is the name given to fibrous tissue accumulation in the skin, which, when it forms elsewhere, is known as fibrosis, but the terms are frequently used interchangeably. The scientific study of fibrosis or scarring was established and developed in skin wounding, as a part of the normal repair response, long before it was appreciated that pathological fibrosis or scarring occurs as a consequence of sustained or iterative injury to internal organs. Increasing experimental evidence indicates that the process of skin wounding with scarring is very similar to the process of organ injury with fibrosis detected in vital organs including the kidney. Kidney fibrosis develops in glomeruli, where it is known as glomerulosclerosis (literally hardening of glomeruli due to fibrotic tissue), or in the interstitial virtual space between tubules and peritubular capillaries, known as interstitial fibrosis. Increasingly fibrosis of the kidney and the cells that make fibrous tissue are seen as targets for therapeutic intervention in chronic diseases of the kidney.
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44

Weimbs, Thomas. Methods in Kidney Cell Biology. Elsevier Science & Technology, 2019.

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45

D'Amico, G., Luigi Minetti, and G. Ponticelli. Kidney in Plasma Cell Dyscrasias. Springer London, Limited, 2012.

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46

Figlin, Robert A., Ronald M. Bukowski, and Robert J. Motzer. Renal Cell Carcinoma: Molecular Targets and Clinical Applications. Springer, 2014.

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47

Figlin, Robert A., Ronald M. Bukowski, and Robert J. Motzer. Renal Cell Carcinoma: Molecular Targets and Clinical Applications. Springer, 2014.

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48

Figlin, Robert A., Ronald M. Bukowski, and Robert J. Motzer. Renal Cell Carcinoma: Molecular Targets and Clinical Applications. Springer New York, 2016.

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49

Renal Cell Carcinoma: Molecular Targets And Clinical Applications. 2nd ed. Humana Press, 2008.

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50

Novick, Andrew, and Ronald M. Bukowski. Renal Cell Carcinoma: Molecular Biology, Immunology, and Clinical Management. Humana Press, 2000.

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