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Relevant bibliographies by topics / Tubular epithelial cell

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Academic literature on the topic 'Tubular epithelial cell'

Author: Grafiati

Published: 5 April 2025

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Journal articles on the topic "Tubular epithelial cell"

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Oberley, T. D., A. H. Yang, and J. Gould-Kostka. "Selection of kidney cell types in primary glomerular explant outgrowths by in vitro culture conditions." Journal of Cell Science 84, no. 1 (1986): 69–92. http://dx.doi.org/10.1242/jcs.84.1.69.

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Adult guinea pig glomeruli were grown in vitro either in serum or in a chemically defined medium. Glomeruli were plated either directly into plastic flasks or into plastic flasks that had been coated with the extracellular matrix produced by the PF-HR-9 mouse teratocarcinoma endodermal cell line. Both the composition of the medium and the nature of the culture substrate affected whole glomerular attachment and the type of cells produced in culture. Quantitative studies demonstrated selection of cell types by different culture conditions. Three colony types, each composed of distinctive cell ty

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Liu, Lele, Yuanjun Deng, Yang Cai, et al. "Ablation of Gsa impairs renal tubule proliferation after injury via CDK2/cyclin E." American Journal of Physiology-Renal Physiology 318, no. 3 (2020): F793—F803. http://dx.doi.org/10.1152/ajprenal.00367.2019.

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Acute kidney injury has a high global morbidity associated with an increased risk of death and chronic kidney disease. Renal tubular epithelial cell regeneration following injury may be a decisive factor in renal repair or the progression of acute kidney injury to chronic kidney disease, but the underlying mechanism of abnormal renal tubular repair remains unclear. In the present study, we investigated the role of heterotrimeric G stimulatory protein α-subunit (Gsa) in renal tubular epithelial cell regeneration. We generated renal tubule epithelium-specific Gsa knockout (GsaKspKO) mice to show

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Breda, Philippe Christophe, Thorsten Wiech, Catherine Meyer-Schwesinger, et al. "Renal proximal tubular epithelial cells exert immunomodulatory function by driving inflammatory CD4+ T cell responses." American Journal of Physiology-Renal Physiology 317, no. 1 (2019): F77—F89. http://dx.doi.org/10.1152/ajprenal.00427.2018.

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In immune-mediated glomerular diseases like crescentic glomerulonephritis (cGN), inflammatory CD4+ T cells accumulate within the tubulointerstitial compartment in close contact to proximal and distal tubular epithelial cells and drive renal inflammation and tissue damage. However, whether renal epithelial cell populations play a role in the pathogenesis of cGN by modulating CD4+ T cell responses is less clear. In the present study, we aimed to investigate the potential of renal epithelial cells to function as antigen-presenting cells, thereby stimulating CD4+ T cell responses. Using a FACS-bas

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TANG, Sydney, Kwok-Wah CHAN, Tak-Mao CHAN, and Kar-Neng LAI. "Sloughing renal tubular epithelial cell." Hong Kong Journal of Nephrology 4, no. 1 (2002): 61. http://dx.doi.org/10.1016/s1561-5413(09)60079-x.

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Carlisle, Rachel E., Alana Heffernan, Elise Brimble, et al. "TDAG51 mediates epithelial-to-mesenchymal transition in human proximal tubular epithelium." American Journal of Physiology-Renal Physiology 303, no. 3 (2012): F467—F481. http://dx.doi.org/10.1152/ajprenal.00481.2011.

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Epithelial-to-mesenchymal transition (EMT) contributes to renal fibrosis in chronic kidney disease. Endoplasmic reticulum (ER) stress, a feature of many forms of kidney disease, results from the accumulation of misfolded proteins in the ER and leads to the unfolded protein response (UPR). We hypothesized that ER stress mediates EMT in human renal proximal tubules. ER stress is induced by a variety of stressors differing in their mechanism of action, including tunicamycin, thapsigargin, and the calcineurin inhibitor cyclosporine A. These ER stressors increased the UPR markers GRP78, GRP94, and

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Monteiro, Maria B., Susanne Ramm, Vidya Chandrasekaran, et al. "A High-Throughput Screen Identifies DYRK1A Inhibitor ID-8 that Stimulates Human Kidney Tubular Epithelial Cell Proliferation." Journal of the American Society of Nephrology 29, no. 12 (2018): 2820–33. http://dx.doi.org/10.1681/asn.2018040392.

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BackgroundThe death of epithelial cells in the proximal tubules is thought to be the primary cause of AKI, but epithelial cells that survive kidney injury have a remarkable ability to proliferate. Because proximal tubular epithelial cells play a predominant role in kidney regeneration after damage, a potential approach to treat AKI is to discover regenerative therapeutics capable of stimulating proliferation of these cells.MethodsWe conducted a high-throughput phenotypic screen using 1902 biologically active compounds to identify new molecules that promote proliferation of primary human proxim

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Liukang, Chengyin, Jing Zhao, Jiaxin Tian, et al. "Deciphering infected cell types, hub gene networks and cell-cell communication in infectious bronchitis virus via single-cell RNA sequencing." PLOS Pathogens 20, no. 5 (2024): e1012232. http://dx.doi.org/10.1371/journal.ppat.1012232.

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Infectious bronchitis virus (IBV) is a coronavirus that infects chickens, which exhibits a broad tropism for epithelial cells, infecting the tracheal mucosal epithelium, intestinal mucosal epithelium, and renal tubular epithelial cells. Utilizing single-cell RNA sequencing (scRNA-seq), we systematically examined cells in renal, bursal, and tracheal tissues following IBV infection and identified tissue-specific molecular markers expressed in distinct cell types. We evaluated the expression of viral RNA in diverse cellular populations and subsequently ascertained that distal tubules and collecti

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Djudjaj, Sonja, Panagiotis Kavvadas, Niki Prakoura, et al. "Activation of Notch3 in Renal Tubular Cells Leads to Progressive Cystic Kidney Disease." International Journal of Molecular Sciences 23, no. 2 (2022): 884. http://dx.doi.org/10.3390/ijms23020884.

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Background: Polycystic kidney disease (PKD) is a genetic disorder affecting millions of people worldwide that is characterized by fluid-filled cysts and leads to end-stage renal disease (ESRD). The hallmarks of PKD are proliferation and dedifferentiation of tubular epithelial cells, cellular processes known to be regulated by Notch signaling. Methods: We found increased Notch3 expression in human PKD and renal cell carcinoma biopsies. To obtain insight into the underlying mechanisms and the functional consequences of this abnormal expression, we developed a transgenic mouse model with conditio

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Kazeminia, Sara, and Alfonso Eirin. "Role of mitochondria in endogenous renal repair." Clinical Science 138, no. 15 (2024): 963–73. http://dx.doi.org/10.1042/cs20231331.

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Abstract Renal tubules have potential to regenerate and repair after mild-to-moderate injury. Proliferation of tubular epithelial cells represents the initial step of this reparative process. Although for many years, it was believed that proliferating cells originated from a pre-existing intra-tubular stem cell population, there is now consensus that surviving tubular epithelial cells acquire progenitor properties to regenerate the damaged kidney. Scattered tubular-like cells (STCs) are dedifferentiated adult renal tubular epithelial cells that arise upon injury and contribute to renal self-he

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White, Lindsay R., Jason B. Blanchette, Li Ren, Ali Awn, Kiril Trpkov та Daniel A. Muruve. "The characterization of α5-integrin expression on tubular epithelium during renal injury". American Journal of Physiology-Renal Physiology 292, № 2 (2007): F567—F576. http://dx.doi.org/10.1152/ajprenal.00212.2006.

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The hallmark of progressive chronic kidney disease is the deposition of extracellular matrix proteins and tubulointerstitial fibrosis. Integrins mediate cell-extracellular matrix interaction and may play a role tubular epithelial injury. Murine primary tubular epithelial cells (TECs) express α5-integrin, a fibroblast marker and the natural receptor for fibronectin. Microscopy localized α5-integrin on E-cadherin-positive cells, confirming epithelial expression. The expression of α5-integrin increased in TECs grown on fibronectin and occurred in parallel with an upregulation of α-smooth muscle a

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Dissertations / Theses on the topic "Tubular epithelial cell"

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Neumann, Marc. "Epithelial cell rearrangements during tubular organ formation /." [S.l.] : [s.n.], 2005. http://edoc.unibas.ch/diss/DissB_7371.

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Kipari, Tiina Marika Johanna. "Inflammatory macrophages and renal tubular epithelial cell apoptosis." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29197.

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Macrophages play a key role in renal inflammation and may be cytotoxic to resident cells within tissues. I begin this thesis by examining the effect of macrophages upon the level of apoptosis and proliferation in tubular epithelial cells <i>in vitro</i>. I then went on to examine the role of NO <i>in vivo</i> in the murine model of unilateral ureteric obstruction (UUO) characterised by tubular cell apoptosis and interstitial fibrosis. The specific iNOS inhibitor L-NIL (control D-NIL) was administered between days 5 to 7 following UUO. Mice were sacrificed at day 7 and the obstructed kidney rem

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Tang, Chi-wai Sydney, and 鄧智偉. "The many facets of the renal proximal tubular epithelial cell inhuman." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31992468.

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Tang, Chi-wai Sydney. "The many facets of the renal proximal tubular epithelial cell in human." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31992468.

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Meimaridou, Eirini. "Calcium oxalate modulation of tubular epithelial cell mitochondria : oxidative vulnerability due to restricted glutathione homeostasis." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444828/.

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Calcium oxalate (COM) crystals are the commonest component of kidney stones. These arise mainly in the distal tubules and collecting ducts. To gain further insight for the cellular damage in terms of oxidative stress caused by COM deposition, in vitro and in vivo model studies were performed. In vitro In renal distal tubule cells, COM and free oxalate treatment caused a 3- and 2-fold increase respectively in superoxide (O2*") formation, originating from mitochondria. This was measured by lucigenin chemiluminescence in digitonin permeabilised cells. However, hydroxyapatite produced a much lower

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Machiguchi, Toshihiko. "Cellular interactions via conditioned media induce in vivo nephron generation from tubular epithelial cells or mesenchymal stem cells." Kyoto University, 2014. http://hdl.handle.net/2433/189325.

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Ashman, Neil. "L-Arginine Transport and Metabolism in an In Vivo Model of Proteinuric Proximal Tubular Epithelial Cell Injury." Thesis, Queen Mary, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498591.

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Li, Moying [Verfasser], and Hans-Joachim [Akademischer Betreuer] Anders. "Mdm2 prevents spontaneous tubular epithelial cell death and acute kidney injury / Moying Li ; Betreuer: Hans-Joachim Anders." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1186629444/34.

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Gallagher, Hugh. "Megalin, cubilin and the proximal tubular epithelial cell : extracellular and intracellular interactions and their relevance to the progression of chronic renal disease." Thesis, St George's, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416020.

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Breda, Philippe Christophe [Verfasser]. "Renal proximal tubular epithelial cells exert immunomodulatory function by driving inflammatory CD4+ T cell responses : Renale proximale Tubulusepithelzellen üben durch Auslösen von inflammatorischen T-Zell-Antworten eine immunmodulatorische Funktion aus / Philippe Christophe Breda." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2020. http://d-nb.info/1221276344/34.

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Books on the topic "Tubular epithelial cell"

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

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

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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, a

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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

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Srisawat, Nattachai, and John A. Kellum. Promoting renal recovery in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0379.

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Better understanding the process of renal recovery following acute kidney injury (AKI) is one of the key steps in improving AKI outcome. We are still lacking the standard definition of renal recovery. Recent progress on the pathophysiology of renal injury and recovery is encouraging. Repopulation of surviving renal tubular epithelial cells with the assistance of certain renal epithelial cell and specific growth factors, play a major role in the recovery process. Moreover, accurate prediction would help physicians distinguish patients with poor renal prognosis in whom further therapy is likely

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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

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Chapman, Hannah, and Christine Elwell. Renal and bladder cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0167.

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This chapter addresses the diagnosis and management of bladder and renal cancers. In the UK, bladder cancer is the fourth most common cancer in men, and the eighth most common cancer in women. Bladder cancer arises from the bladder urothelium, and is typically a papillary transitional cell carcinoma. Chronic infection with the parasite Schistosoma haematobium is associated with squamous cell carcinoma of the bladder, and is most prevalent in Egypt and sub-Saharan Africa. Renal cancer accounts for 3% of cancers in adults in the UK and, in most cases, is a renal cell carcinoma arising from proxi

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Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.

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The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistrie

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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

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Servais, Aude, and Bertrand Knebelmann. Cystinuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0024.

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Cystinuria (OMIM #220100) is an autosomal recessive disorder of a dibasic amino acid transport in the apical membrane of epithelial cells of the renal proximal tubule and small intestine. It leads to increased urinary cystine excretion and recurrent urolithiasis. The cystine transporter is an heterodimeric transporter which is composed of a heavy subunit, rBAT, linked to a light subunit, b0,+AT. Two genes, SLC3A1 (solute carrier family 3 member 1) and SLC7A9, coding for rBAT and b0,+AT, account for the genetic basis of cystinuria. Cystinuria may lead to obstruction, infections, and ultimately

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Daudon, Michel, and Paul Jungers. Cystine stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0203_update_001.

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Cystinuria, an autosomal recessive disease (estimated at 1:7000 births worldwide), results from the defective reabsorption of cystine and dibasic amino acids (also ornithine, arginine, lysine, COAL) by epithelial cells of renal proximal tubules, leading to an abnormally high urinary excretion of these amino acids. Due to the poor solubility of cystine at the usual urine pH, formation of cystine crystals and stones ensues. Incidence of homozygotes is estimated at 1 in 7000 births worldwide, but is lower in European countries and much higher in populations with frequent consanguinity. Cystine st

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Book chapters on the topic "Tubular epithelial cell"

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Liu, Bi-Cheng, Tao-Tao Tang, and Lin-Li Lv. "How Tubular Epithelial Cell Injury Contributes to Renal Fibrosis." In Advances in Experimental Medicine and Biology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2_11.

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Condorelli, L., I. Cattaneo, C. Arrigoni, L. Antiga, N. Perico, and A. Remuzzi. "Effect of fluid shear stress on tubular kidney epithelial cell structure." In IFMBE Proceedings. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03900-3_15.

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Zink, Sabrina, and Ralf Jacob. "Tubulin Detyrosination in Epithelial Cells." In The Cytoskeleton in Health and Disease. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2904-7_8.

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Sepúlveda, Francisco V., and Jeremy D. Pearson. "Amino Acid Transport in Cultured Kidney Tubule Cells." In Tissue Culture of Epithelial Cells. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_6.

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Larsen, Erik Hviid, and Jens Nørkær Sørensen. "Stationary and Nonstationary Ion and Water Flux Interactions in Kidney Proximal Tubule: Mathematical Analysis of Isosmotic Transport by a Minimalistic Model." In Reviews of Physiology, Biochemistry and Pharmacology. Springer International Publishing, 2019. http://dx.doi.org/10.1007/112_2019_16.

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AbstractOur mathematical model of epithelial transport (Larsen et al. Acta Physiol. 195:171–186, 2009) is extended by equations for currents and conductance of apical SGLT2. With independent variables of the physiological parameter space, the model reproduces intracellular solute concentrations, ion and water fluxes, and electrophysiology of proximal convoluted tubule. The following were shown: Water flux is given by active Na+ flux into lateral spaces, while osmolarity of absorbed fluid depends on osmotic permeability of apical membranes. Following aquaporin “knock-out,” water uptake is not reduced but redirected to the paracellular pathway. Reported decrease in epithelial water uptake in aquaporin-1 knock-out mouse is caused by downregulation of active Na+ absorption. Luminal glucose stimulates Na+ uptake by instantaneous depolarization-induced pump activity (“cross-talk”) and delayed stimulation because of slow rise in intracellular [Na+]. Rate of fluid absorption and flux of active K+ absorption would have to be attuned at epithelial cell level for the [K+] of the absorbate being in the physiological range of interstitial [K+]. Following unilateral osmotic perturbation, time course of water fluxes between intraepithelial compartments provides physical explanation for the transepithelial osmotic permeability being orders of magnitude smaller than cell membranes’ osmotic permeability. Fluid absorption is always hyperosmotic to bath. Deviation from isosmotic absorption is increased in presence of glucose contrasting experimental studies showing isosmotic transport being independent of glucose uptake. For achieving isosmotic transport, the cost of Na+ recirculation is predicted to be but a few percent of the energy consumption of Na+/K+ pumps.

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Trump, Benjamin F., and Irene K. Berezesky. "Ion Deregulation in Injured Proximal Tubule Epithelial Cells." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_113.

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Bowman, B. B., and D. B. McCormick. "Pyriloxine Uptake by Proximal Tubular Epithelial Cells Isolated from Rat Kidney." In Biochemistry of Vitamin B6. Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-9308-4_72.

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Bertelli, R., F. Ginevri, P. Altieri, A. Garberi, G. M. Ghiggeri, and R. Gusmano. "Morphological and Biochemical Characteristics of Human Tubular Epithelial Cells “In Culture” Deriving from Nephronophthisis." In Tubulo-Interstitial Nephropathies. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3892-9_36.

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Feng, Ying, Shumei Lin, Xiaoyan Zhao, et al. "Taurine Inhibited Uric Acid Uptake in HK-2 Renal Tubular Epithelial Cells." In Advances in Experimental Medicine and Biology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8023-5_13.

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Du, Caigan, Ximo Wang, and Huifang Chen. "Oxidative Stress to Renal Tubular Epithelial Cells – A Common Pathway in Renal Pathologies." In Systems Biology of Free Radicals and Antioxidants. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_187.

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Conference papers on the topic "Tubular epithelial cell"

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Kumar, Balawant, Rizwan Ahmad, Pinelopi Kapitsino, et al. "Abstract 1767: Rho-GTPase inhibits claudin-2 expression to promote proximal tubular epithelial cell plasticity and renal cell carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1767.

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Kumar, Balawant, Rizwan Ahmad, Pinelopi Kapitsino, et al. "Abstract 1767: Rho-GTPase inhibits claudin-2 expression to promote proximal tubular epithelial cell plasticity and renal cell carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1767.

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Soni, Abhishek, Nupur Bansal, A. K. Dhull, Vivek Kaushal, Rajeev Atri, and Monica Verma. "Diagnostic dilemma of mesonephric adenocarcinoma cervix." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685283.

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Introduction: Mesonephric carcinoma is a rare type of epithelial tumor of the uterine cervix which derive from the remnants of the paired mesonephric (Wolff’s) ducts. The incidence of such neoplasms is difficult to determine due to rarity, previous misclassification of clear cell carcinomas and yolk sac tumours as mesonephric carcinomas and potential underreporting due to misclassification of mesonephric carcinoma as Mullerian tumours or mesonephric hyperplasia. The evidence regarding the clinical course, prognosis and optimal treatment is limited. Materials and Methods: Searches were performe

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Liu, Haijun, Xiaoyan Cai, Lie Dai, MA Jianda, Yingqian Mo, and Minyan Xie. "FRI0226 LOW EXPRESSION OF ESTROGEN RECEPTOR BETA IN RENAL TUBULAR EPITHELIAL CELL MAY CONTRIBUTE TO HYPERURICEMIA IN PREMENOPAUNITED STATES OF AMERICAL FEMALE SYSTEMIC LUPUS ERYTHEMATOSUS PATIENTS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3586.

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Wang, Jianbin, Jinseok Heo, and Susan Z. Hua. "Development of Microfluidic Chips to Study the Effects of Shear Stress on Cell Functions." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13132.

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Fluid shear stress has profound effect on many cell functions, including proliferation, migration, transport, and gene expression. Cellular systems such as endothelial cells in heart artery and epithelial cells in kidney tubule are constantly subject to fluid flow. We have developed a series of microfluidic chips that generate a wide range and modes of shear stresses within a perfusion chamber, enabling us to culture cells on chip and examine the effects of shear stress on cell growth and cell functions.

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Kaewpaiboon, Sunisa, Titpawan Nakpheng, and Teerapol Srichana. "Biocompatibility of Polymyxin B Sulfate Based on Sodium Deoxycholate Sulfate Formulations with Kidney Cell Lines, Macrophage Cells, and Red Blood Cells." In 5th International Conference and Exhibition on Pharmaceutical Sciences and Technology 2022. Trans Tech Publications Ltd, 2022. http://dx.doi.org/10.4028/p-7490x3.

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Antibiotic-resistant has emerged without new drug challenges. Polymyxin B (PMB) was the last resort therapy for multiple-drug resistant Gram-negative bacteria. However, the toxicity of PMB including nephrotoxicity (61%) and neurotoxicity (7%) was dose-limitation. PMB-based sodium deoxycholate sulfate (SDCS) formulations were prepared in the 2-different mole ratios of SDCS to PMB (5:1 and 10:1). Particle size, zeta-potential, and drug content were evaluated. The biocompatibility of PMB formulations was investigated with normal human primary renal proximal tubule epithelial cells (PCS-400-010),

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Al Meselmani, M. A., та N. A. Glinskaya. "ANALYSIS OF MORPHOLOGICAL CHANGES OF TESTES AFTER γ- IRRADIA-TION". У NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.183-184.

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We studied the effects of radiation in small doses (0.5 Gy) on the spermatogenic epithelium of white rats, counted the number of transversely cut convoluted seminiferous tubules, and de-termined the types of tubules. A decrease in the number of seminiferous tubules was noted, with damage to the cells of the spermatogenic epithelium.

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Lee, Gi-Ja, Ji-Hye Kim, Hun-Kuk Park, Kyung-Hwan Jeong, Hyun-Jung Kang, and Tae Won Lee. "Observation of angiotensin II-induced changes in tubular epithelial cells utilizing AFM: Angiotensin II-induced changes in tubular cells." In 2010 IEEE 4th International Conference on Nano/Molecular Medicine and Engineering (NANOMED). IEEE, 2010. http://dx.doi.org/10.1109/nanomed.2010.5749834.

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GUO, Da, Jian-min WANG, and Jian-ming OUYANG. "Injured Human Kidney Proximal Tubular Epithelial Cells Modulate Nucleation and Growth of Calcium Oxalate Crystals." In 2nd International Conference on Biomedical and Biological Engineering 2017 (BBE 2017). Atlantis Press, 2017. http://dx.doi.org/10.2991/bbe-17.2017.27.

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Lagies, Simon, Soeren Lienkamp, Bernd Kammerer, et al. "Directly reprogrammed renal tubular epithelial cells are sensitive to typical metabolic alterations occurring in hyperglycemia." In The 2nd International Electronic Conference on Metabolomics. MDPI, 2017. http://dx.doi.org/10.3390/iecm-2-04991.

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Reports on the topic "Tubular epithelial cell"

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Pines, Mark, Arieh Bar, David A. Carrino, Arnold I. Caplan, and James A. Dennis. Extracellular Matrix Molecules of the Eggshell as Related to Eggshell Quality. United States Department of Agriculture, 1997. http://dx.doi.org/10.32747/1997.7575270.bard.

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The extracellular matrix of the mineralizing eggshell contains molecules hypothesized to be regulators biomineralization. To study eggshell matrix molecules, a bank of monoclonal antibodies was generated that bound demineralized eggshell matrix or localized to oviduct epithelium. Immunofluorescence staining revealed several staining patterns for antibodies that recognized secretory cells: staining for a majority of columnar lining cells, staining for a minor sub-set of columnar lining cells, intensified staining within epithelial crypts, and staining of the entire tubular gland. Western blotti

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