Relevant bibliographies by topics / Kidney epithelial cells

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Kidney epithelial cells'

Author: Grafiati
Published: 22 June 2024
Last updated: 31 July 2025

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Journal articles on the topic "Kidney epithelial cells"

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Verghese, George M., Michael F. Gutknecht, and George H. Caughey. "Prostasin regulates epithelial monolayer function: cell-specific Gpld1-mediated secretion and functional role for GPI anchor." American Journal of Physiology-Cell Physiology 291, no. 6 (2006): C1258—C1270. http://dx.doi.org/10.1152/ajpcell.00637.2005.

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Prostasin, a trypsinlike serine peptidase, is highly expressed in prostate, kidney, and lung epithelia, where it is bound to the cell surface, secreted, or both. Prostasin activates the epithelial sodium channel (ENaC) and suppresses invasion of prostate and breast cancer cells. The studies reported here establish mechanisms of membrane anchoring and secretion in kidney and lung epithelial cells and demonstrate a critical role for prostasin in regulating epithelial monolayer function. We report that endogenous mouse prostasin is glycosylphosphatidylinositol (GPI) anchored to the cell surface a
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Pastor-Soler, Núria M., Timothy A. Sutton, Henry E. Mang, et al. "Muc1 is protective during kidney ischemia-reperfusion injury." American Journal of Physiology-Renal Physiology 308, no. 12 (2015): F1452—F1462. http://dx.doi.org/10.1152/ajprenal.00066.2015.

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Ischemia-reperfusion injury (IRI) due to hypotension is a common cause of human acute kidney injury (AKI). Hypoxia-inducible transcription factors (HIFs) orchestrate a protective response in renal endothelial and epithelial cells in AKI models. As human mucin 1 (MUC1) is induced by hypoxia and enhances HIF-1 activity in cultured epithelial cells, we asked whether mouse mucin 1 (Muc1) regulates HIF-1 activity in kidney tissue during IRI. Whereas Muc1 was localized on the apical surface of the thick ascending limb, distal convoluted tubule, and collecting duct in the kidneys of sham-treated mice
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Kim, Bo Hye, Do Yeon Kim, Yejin Ahn, et al. "Semaphorin-3C Is Upregulated in Polycystic Kidney Epithelial Cells and Inhibits Angiogenesis of Glomerular Endothelial Cells." American Journal of Nephrology 51, no. 7 (2020): 556–64. http://dx.doi.org/10.1159/000508263.

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Background: Polycystic kidney disease (PKD) is a hereditary disease characterized by cyst formation in the kidneys bilaterally. It has been observed that semaphorin-3C (SEMA3C) is overexpressed in polycystic kidney epithelial cells. It is hypothesized that upregulated SEMA3C would contribute to survival of polycystic kidney epithelial cells. Furthermore, as the kidney is a highly vascularized organ, the secreted SEMA3C from PKD epithelial cells will affect glomerular endothelial cells (GECs) in a paracrine manner. Methods: To evaluate the effect of SEMA3C on renal cells, siSEMA3C-treated PKD e
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TUFRO, ALDA, VICTORIA F. NORWOOD, ROBERT M. CAREY, and R. ARIEL GOMEZ. "Vascular Endothelial Growth Factor Induces Nephrogenesis and Vasculogenesis." Journal of the American Society of Nephrology 10, no. 10 (1999): 2125–34. http://dx.doi.org/10.1681/asn.v10102125.

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Abstract. The expression of vascular endothelial growth factor (VEGF) and its receptors Flt-1 and Flk-1 in the rat kidney was examined during ontogeny using Northern blot analysis and immunocytochemistry. In prevascular embryonic kidneys (embryonic day 14 [E14]), immunoreactive Flt-1 and Flk-1 were observed in isolated angioblasts, whereas VEGF was not detected. Angioblasts aligned forming cords before morphologically differentiating into endothelial cells. In late fetal kidneys (E19), immunoreactive VEGF was detected in glomerular epithelial and tubular cells, whereas Flt-1 and Flk-1 were exp
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Cramer, E. B., L. C. Milks, M. J. Brontoli, G. K. Ojakian, S. D. Wright, and H. J. Showell. "Effect of human serum and some of its components on neutrophil adherence and migration across an epithelium." Journal of Cell Biology 102, no. 5 (1986): 1868–77. http://dx.doi.org/10.1083/jcb.102.5.1868.

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The effect of human serum and some of its components on the process of transepithelial migration of human neutrophils was investigated in an in vitro system. 10% autologous serum caused an increase in neutrophil adherence to and migration across canine kidney epithelial cells. This increase in neutrophil binding also occurred if the epithelium but not the neutrophils had been preincubated with serum. The binding was lost if the serum was either preabsorbed over the kidney epithelium before use or heat inactivated. Indirect immunofluorescence studies indicated that IgG, IgM, and a component of
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Dahl, Ulf, Anders Sjödin, Lionel Larue, et al. "Genetic Dissection of Cadherin Function during Nephrogenesis." Molecular and Cellular Biology 22, no. 5 (2002): 1474–87. http://dx.doi.org/10.1128/mcb.22.5.1474-1487.2002.

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ABSTRACT The distinct expression of R-cadherin in the induced aggregating metanephric mesenchyme suggests that it may regulate the mesenchymal-epithelial transition during kidney development. To address whether R-cadherin is required for kidney ontogeny, R-cadherin-deficient mice were generated. These mice appeared to be healthy and were fertile, demonstrating that R-cadherin is not essential for embryogenesis. The only kidney phenotype of adult mutant animals was the appearance of dilated proximal tubules, which was associated with an accumulation of large intracellular vacuoles. Morphologica
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Pat, Betty, David W. Johnson, and Glenda C. Gobe. "Role of JAK3 in the Pathogenesis of Oxidative Stress-Induced Kidney Fibrosis." Journal of Renal and Hepatic Disorders 2, no. 1 (2018): 18–26. http://dx.doi.org/10.15586/jrenhep.2018.30.

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The Janus kinase (JAK) tyrosine kinase family and JAK/STAT signal transduction pathway may act in kidney fibrogenesis. JAK3 expression was investigated in in vitro and in vivo models of kidney fibrosis involving oxidative stress. There was a marked down-regulation of JAK3 mRNA in rat kidney tubular epithelial cells (NRK52E) and fibroblasts (NRK49F) exposed to 1.0 mM H2O2 for 18–20 h compared with controls, which correlated with increased apoptosis and decreased mitosis in both cell lines. However, JAK3 protein levels were not significantly different in control and H2O2-treated epithelial and f
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Kuberka, M., G. Rau, and B. Glasmacher. "CRYOPRESERVATION OF EPITHELIAL KIDNEY CELLS." Biomedizinische Technik/Biomedical Engineering 48, s1 (2003): 322–23. http://dx.doi.org/10.1515/bmte.2003.48.s1.322.

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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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Sorokin, L., A. Sonnenberg, M. Aumailley, R. Timpl, and P. Ekblom. "Recognition of the laminin E8 cell-binding site by an integrin possessing the alpha 6 subunit is essential for epithelial polarization in developing kidney tubules." Journal of Cell Biology 111, no. 3 (1990): 1265–73. http://dx.doi.org/10.1083/jcb.111.3.1265.

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It has been previously shown that A-chain and domain(E8)-specific antibodies to laminin that inhibit cell adhesion also interfere with the establishment of epithelial cell polarity during kidney tubule development (Klein, G., M. Langegger, R. Timpl, and P. Ekblom. 1988. Cell. 55:331-341). A monoclonal antibody specific for the integrin alpha 6 subunit, which selectively blocks cell binding to E8, was used to study the receptors involved. Immunofluorescence staining of embryonic kidneys and of organ cultures of metanephric mesenchyme demonstrated coappearance of the integrin alpha 6 subunit and
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Dissertations / Theses on the topic "Kidney epithelial cells"

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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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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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Measures, H. R. "A study of desmosome formation in kidney epithelial cells." Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234435.

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Xie, Jianxun. "Involvement of transcription factors in cadmium-induced apoptosis and cell cycle arrest in rat kidney cells /." View online ; access limited to URI, 2005. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3206258.

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Lim, Ai Ing, and 林艾盈. "Shedding of kidney injury molecule-1 by kidney proximal tubular epithelial cells: the role of matrixmetalloproteinase-3." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49799745.

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Regardless of the original cause and etiology, the progression of kidney disease follows a final common pathway associated with tubulointerstitial injury, in which proximal tubular epithelial cells (PTEC) are instrumental. Kidney injury molecule-1 (KIM-1) is an emerging biomarker of kidney tubular damage. It is markedly expressed and released into urine in various animal models and human kidney diseases. This study aimed to explore the underlying mechanism regulating the release of KIM-1 by PTEC. First, expression and release of KIM-1 by primary cultured human PTEC were examined. In quiesc
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Zhou, Li. "The molecular mechanisms of aristolochic acid nephropathy." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43224349.

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Laestadius, Åsa. "Cellular mechanisms of interaction between uropathogenic Escherichia coli and renal epithelial cells /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-187-X.

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Sampangi, Sandeep. "Autologous human kidney proximal tubule epithelial cells (PTEC) modulate dendritic cell (DC), T cell and B cell responses." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/82033/1/Sandeep_Sampangi_Thesis.pdf.

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This is a comprehensive study of human kidney proximal tubular epithelial cells (PTEC) which are known to respond to and mediate the pathological process of a range of kidney diseases. It identifies various molecules expressed by PTEC and how these molecules participate in down-regulating the inflammatory process, thereby highlighting the clinical potential of these molecules to treat various kidney diseases. In the disease state, PTEC gain the ability to regulate the immune cell responses present within the interstitium. This down-regulation is a complex interaction of contact dependent/indep
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Broadbelt, Nalini V. "Regulation of iNOS expression : in response to pressure in proximal tubule epithelial cells /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1619205731&sid=2&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Miskovic, Dragana. "A characterization of BiP gene expression in Xenopus laevis embryos and A6 kidney epithelial cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/NQ38257.pdf.

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Books on the topic "Kidney epithelial cells"

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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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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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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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Marksitzer, René. Mechanism for cAMP-induced, tissue-specific regulation of the urokinase-type plasminogen activator gene in kidney epithelial cells. 1996.

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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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Sebastio, Gianfranco, Manuel Schiff, and Hélène Ogier de Baulny. Lysinuric Protein Intolerance and Hartnup Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0025.

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Lysinuric protein intolerance (LPI) is an inherited aminoaciduria caused by defective cationic amino acid transport at the basolateral membrane of epithelial cells in intestine and kidney. LPI is caused by mutations in the SLC7A7 gene, which encodes the y+LAT-1 protein, the catalytic light chain subunit of a complex belonging to the heterodimeric amino acid transporter family. Symptoms usually begin after weaning with refusal of feeding, vomiting, and consequent failure to thrive. Hepatosplenomegaly, hematological anomalies, and neurological involvement including hyperammonemic coma will progr
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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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Book chapters on the topic "Kidney epithelial cells"

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Sorokin, Lydia, Gerd Klein, Gabriele Mugrauer, Lothar Fecker, Marja Ekblom, and Peter Ekblom. "Development of kidney epithelial cells." In Epithelial Organization and Development. Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2354-9_6.

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Liehr, Joachim G., and David A. Sirbasku. "Estrogen-Dependent Kidney Tumors." In Tissue Culture of Epithelial Cells. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_11.

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Guggino, Sandra. "Channels in Kidney Epithelial Cells." In Ionic Channels in Cells and Model Systems. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5077-4_13.

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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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Kuure, Satu. "Analysis of Migration in Primary Ureteric Bud Epithelial Cells." In Kidney Development. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-851-1_13.

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Saier, Milton H. "Application of the Microbiological Approach to the Study of Passive Monovalent Salt Transport in a Kidney Epithelial Cell Line, MDCK." In Tissue Culture of Epithelial Cells. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_4.

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Leonard, Jack L. "Thyroid Hormone Metabolism in Kidney Epithelial Cells in Continuous Culture." In Frontiers in Thyroidology. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5260-0_77.

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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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Toback, F. Gary, Sreedharan Kartha, and Margaret M. Walsh-Reitz. "Determinants of Autocrine and Paracrine Growth Factor Release by Kidney Epithelial Cells." In Nephrology. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_135.

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Claude-Taupin, Aurore, Nicolas Dupont, and Patrice Codogno. "Shear Stress-Dependent Regulation of Autophagy and Metabolism in Kidney Epithelial Cells." In Learning Materials in Biosciences. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-88121-3_8.

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Conference papers on the topic "Kidney epithelial cells"

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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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Vitol, Elina A., Timothy P. Kurzweg, and Bahram Nabet. "Light scattering properties of kidney epithelial cells and nuclei." In Biomedical Optics 2006, edited by Robert R. Alfano and Alvin Katz. SPIE, 2006. http://dx.doi.org/10.1117/12.644863.

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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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Azeloglu, Evren U., Mark Stothers, Thomas J. Deerinck, et al. "3-D Quantitative Microanatomy of Rat Kidney Podocytes as Determined by Serial Block-Face Scanning Electron Microscopy." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80650.

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The shape of a cell is critical for proper signaling and resultant biological function [1]. Podocytes, kidney visceral epithelial cells, have a distinctive morphology with interdigitating foot processes that wrap around the capillaries of the glomeruli and, together with endothelial cells and the basement membrane, form the glomerular filtration barrier. In addition to forming the filtration barrier, slit diaphragms that connect the alternating foot processes from two podocytes are thought to be signaling hubs that regulate cell morphology and function.
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Loh, Jeremy, Karl Schumacher, Annegret Schumacher, Shyi-Herng Kan, and Jackie Y. Ying. "Engineering Homogeneous Micromagnetic Fields for Cell Patterning." In ASME 2006 International Manufacturing Science and Engineering Conference. ASMEDC, 2006. http://dx.doi.org/10.1115/msec2006-21041.

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Micropatterning of cells was achieved by the application of micromagnetic fields using ferromagnetic field modulators. These modulators were made of low carbon steel, and micromachined using the wire-cut method. They were engineered to disrupt the regular pathways of magnetic flux lines, and create localized regions of micromagnetic fields. Uniform micromagnetic fields were achieved via design evaluation using Maxwell®2D magnetostatic simulations. Application of the micromagnetic field modulators on Madin-Darby canine kidney (MDCK) epithelial cells demonstrated good cell adhesion and uniform c
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Chang, Yu-Wei, and Kamaleshwar Singh. "Abstract 3080: Chronic exposure to arsenic induces malignant transformation in human kidney epithelial cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3080.

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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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Di´az, Rube´n, and Boris Rubinsky. "A Single Cell Study on the Temperature Effects of Electroporation." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61151.

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In electroporation, the charging of the cell membrane due to an applied electric field is followed by a localized structural rearrangement of the membrane, which consequently creates pores or aqueous pathways that perforate the membrane. A tremendous increase in ionic and molecular transport through the membrane occurs because of the presence of these aqueous pores. As part of a comprehensive study on the effects of temperature on electroporation of cells, we have designed a micro device capable of integrating single cells into an electronic circuit while controlling the temperature. In the pr
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Nguyen, Thi-Ngoc, and Tien Hsu. "Abstract B92: VHL inactivated kidney epithelial cells reprogram macrophage behavior through IL-6 and CXCL-1 secretion." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b92.

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10

Chang, Yuwei, and Kamaleshwar Singh. "Abstract 879: Nicotine-induced oxidative stress causes epigenetic alterations during malignant transformation of human kidney epithelial cells." 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.sabcs18-879.

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