Relevant bibliographies by topics / Tubule renal

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  2. Dissertations / Theses
  3. Books
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  5. Conference papers

Academic literature on the topic 'Tubule renal'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Tubule renal"

1

Wen, Donghai, Li Ni, Li You, et al. "Upregulation of nestin in proximal tubules may participate in cell migration during renal repair." American Journal of Physiology-Renal Physiology 303, no. 11 (2012): F1534—F1544. http://dx.doi.org/10.1152/ajprenal.00083.2012.

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The characteristics of renal tubular progenitor/precursor cells and the role of renal tubule regeneration in the repair of remnant kidneys (RKs) after nephrectomy are not well known. In the present study of a murine model of subtotal nephrectomy, we used immunofluorescence (IF), immunoblot analysis, and in situ hybridization methods to demonstrate that nestin expression was transiently upregulated in tubule cells near the incision edges of RKs. The nestin-positive tubules were immature proximal tubules that colabeled with lotus tetragonolobus agglutinin but not with markers of mature tubules (aquaporin-1, Tamm-Horsfall protein, and aquaporin-2). In addition, many of the nestin-expressing tubule cells were actively proliferative cells, as indicated by colabeling with bromodeoxyuridine. Double-label IF and immunoblot analysis also showed that the upregulation of tubular nestin was associated with enhanced transforming growth factor-β1 (TGF-β1) expression in the incision edge of RKs but not α-smooth muscle actin, which is a marker of fibrosis. In cultured human kidney proximal tubule cells (HKC), immunoblot analysis indicated that TGF-β1 induced nestin expression and loss of E-cadherin expression, suggesting an association of nestin expression and cellular dedifferentiation. Knockdown of nestin expression by a short hairpin RNA-containing plasmid led to decreased migration of HKC cells that were induced by TGF-β1. Taken together, our results suggest that the tubule repair that occurs during the recovery process following nephrectomy may involve TGF-β1-induced nestin expression in immature renal proximal tubule cells and the promotion of renal cell migration.
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Pleniceanu, Oren, Orit Harari-Steinberg, Dorit Omer, et al. "Successful Introduction of Human Renovascular Units into the Mammalian Kidney." Journal of the American Society of Nephrology 31, no. 12 (2020): 2757–72. http://dx.doi.org/10.1681/asn.2019050508.

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BackgroundCell-based therapies aimed at replenishing renal parenchyma have been proposed as an approach for treating CKD. However, pathogenic mechanisms involved in CKD such as renal hypoxia result in loss of kidney function and limit engraftment and therapeutic effects of renal epithelial progenitors. Jointly administering vessel-forming cells (human mesenchymal stromal cells [MSCs] and endothelial colony-forming cells [ECFCs]) may potentially result in in vivo formation of vascular networks.MethodsWe administered renal tubule–forming cells derived from human adult and fetal kidneys (previously shown to exert a functional effect in CKD mice) into mice, alongside MSCs and ECFCs. We then assessed whether this would result in generation of “renovascular units” comprising both vessels and tubules with potential interaction.ResultsDirectly injecting vessel-forming cells and renal tubule–forming cells into the subcutaneous and subrenal capsular space resulted in self-organization of donor-derived vascular networks that connected to host vasculature, alongside renal tubules comprising tubular epithelia of different nephron segments. Vessels derived from MSCs and ECFCs augmented in vivo tubulogenesis by the renal tubule–forming cells. In vitro coculture experiments showed that MSCs and ECFCs induced self-renewal and genes associated with mesenchymal–epithelial transition in renal tubule–forming cells, indicating paracrine effects. Notably, after renal injury, renal tubule–forming cells and vessel-forming cells infused into the renal artery did not penetrate the renal vascular network to generate vessels; only administering them into the kidney parenchyma resulted in similar generation of human renovascular units in vivo.ConclusionsCombined cell therapy of vessel-forming cells and renal tubule–forming cells aimed at alleviating renal hypoxia and enhancing tubulogenesis holds promise as the basis for new renal regenerative therapies.
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Romero, Cesar A., and Oscar A. Carretero. "Tubule-vascular feedback in renal autoregulation." American Journal of Physiology-Renal Physiology 316, no. 6 (2019): F1218—F1226. http://dx.doi.org/10.1152/ajprenal.00381.2018.

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Afferent arteriole (Af-Art) diameter regulates pressure and flow into the glomerulus, which are the main determinants of the glomerular filtration rate. Thus, Af-Art resistance is crucial for Na+ filtration. Af-Arts play a role as integrative centers, where systemic and local systems interact to determine the final degree of resistance. The tubule of a single nephron contacts an Af-Art of the same nephron at two locations: in the transition of the thick ascending limb to the distal tubule (macula densa) and again in the connecting tubule. These two sites are the anatomic basis of two intrinsic feedback mechanisms: tubule-glomerular feedback and connecting tubule-glomerular feedback. The cross communications between the tubules and Af-Arts integrate tubular Na+ and water processing with the hemodynamic conditions of the kidneys. Tubule-glomerular feedback provides negative feedback that tends to avoid salt loss, and connecting tubule-glomerular feedback provides positive feedback that favors salt excretion by modulating tubule-glomerular feedback (resetting it) and increasing glomerular filtration rate. These feedback mechanisms are also exposed to systemic modulators (hormones and the nervous system); however, they can work in isolated kidneys or nephrons. The exaggerated activation or absence of any of these mechanisms may lead to disequilibrium in salt and water homeostasis, especially in extreme conditions (e.g., high-salt diet/low-salt diet) and may be part of the pathogenesis of some diseases. In this review, we focus on molecular signaling, feedback interactions, and the physiological roles of these two feedback mechanisms.
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Lee, H. Thomas, Michael Jan, Soo Chan Bae, et al. "A1 adenosine receptor knockout mice are protected against acute radiocontrast nephropathy in vivo." American Journal of Physiology-Renal Physiology 290, no. 6 (2006): F1367—F1375. http://dx.doi.org/10.1152/ajprenal.00347.2005.

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The role of renal A1 adenosine receptors (A1AR) in the pathogenesis of radiocontrast nephropathy is controversial. We aimed to further elucidate the role of A1AR in the pathogenesis of radiocontrast nephropathy and determine whether renal proximal tubule A1AR contribute to the radiocontrast nephropathy. To induce radiocontrast nephropathy, A1AR wild-type (WT) or knockout (KO) mice were injected with a nonionic radiocontrast (iohexol, 1.5–3 g iodine/kg). Some A1WT mice were pretreated with 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; a selective A1AR antagonist) before iohexol injection. A1AR contribute to the pathogenesis of radiocontrast nephropathy in vivo as the A1WT mice developed significantly worse acute renal failure, more renal cortex vacuolization, and had lower survival 24 h after iohexol treatment compared with the A1KO mice. DPCPX pretreatment also protected the A1WT mice against radiocontrast-induced acute renal failure. No differences in renal cortical apoptosis or inflammation were observed between A1WT and A1KO mice. To determine whether the proximal tubular A1AR mediate the direct renal cytotoxicity of radiocontrast, we treated proximal tubules in culture with iohexol with or without 2-chloro- N6-cyclopentyladenosine (a selective A1AR agonist) or DPCPX pretreatment. We also subjected cultured proximal tubule cells overexpressing A1AR or lacking A1AR to radiocontrast injury. Iohexol caused a direct dose-dependent reduction in proximal tubule cell viability as well as proliferation. Neither the A1AR agonist nor the antagonist treatment affected proximal tubule viability or proliferation. Moreover, overexpression or lack of A1AR failed to impact the iohexol toxicity on proximal tubule cells. Therefore, we conclude that radiocontrast causes acute renal failure via mechanisms dependent on A1AR; however, renal proximal tubule A1AR do not contribute to the direct tubular toxicity of radiocontrast.
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Maurel, Agnès, Odile Spreux-Varoquaux, Francesco Amenta, et al. "Vesicular monoamine transporter 1 mediates dopamine secretion in rat proximal tubular cells." American Journal of Physiology-Renal Physiology 292, no. 5 (2007): F1592—F1598. http://dx.doi.org/10.1152/ajprenal.00514.2006.

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Renal dopamine, synthesized by proximal tubules, plays an important role in the regulation of renal sodium excretion. Although the renal dopaminergic system has been extensively investigated in both physiological and pathological situations, the mechanisms whereby dopamine is stored and secreted by proximal tubule cells remain obscure. In the present study we investigated whether vesicular monoamine transporters (VMAT)-1 and -2, which participate in amine storing and secretion, are expressed in rat renal proximal tubules, and we defined their involvement in dopamine secretion. By combining RT-PCR, Western blot, and immunocytochemistry we showed that VMAT-1 is the predominant isoform expressed in isolated proximal tubule cells. These results were confirmed by immunohistochemistry analysis of rat renal cortex showing that VMAT-1 was found in proximal tubules but not in glomeruli. Functional studies showed that, as previously reported for VMAT-dependent amine transporters, dopamine release by cultured proximal tubule cells was partially inhibited by disruption of intracellular H+ gradient. In addition, dopamine secretion was prevented by the VMAT-1/VMAT-2 inhibitor reserpine but not by the VMAT-2 inhibitor tetrabenazine. Finally, we demonstrated that tubular VMAT-1 mRNA and protein expression were significantly upregulated during a high-sodium diet. In conclusion, our results show for the first time the expression of a VMAT in the renal proximal tubule and its involvement in regulation of dopamine secretion. These data represent the first step toward the comprehension of the role of this transporter in renal dopamine handling and its involvement in pathological situations.
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Ramachandran, C., and M. G. Brunette. "The renal Na+/Ca2+ exchange system is located exclusively in the distal tubule." Biochemical Journal 257, no. 1 (1989): 259–64. http://dx.doi.org/10.1042/bj2570259.

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The movement of Ca2+ across the basolateral plasma membrane was determined in purified preparations of this membrane isolated from rabbit proximal and distal convoluted tubules. The ATP-dependent Ca2+ uptake was present in basolateral membranes from both these tubular segments, but the activity was higher in the distal tubules. A very active Na+/Ca2+ exchange system was also demonstrated in the distal-tubular membranes, but in proximal-tubular membranes this exchange system was not demonstrable. The presence of Na+ outside the vesicles gradually inhibited the ATP-dependent Ca2+ uptake in the distal-tubular-membrane preparations, but remained without effect in those from the proximal tubules. The activity of the Na+/Ca2+ exchange system in the distal-tubular membranes was a function of the imposed Na+ gradient. These results suggest that the major differences in the characteristics of Ca2+ transport in the proximal and in the distal tubules are due to the high activity of a Na+/Ca2+ exchange system in the distal tubule and its virtual absence in the proximal tubule.
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MacLaughin, M., and M. Mello Aires. "Renal Acidification Defect Induced by Lithium in Control and Acidotic Rats." Clinical Science 79, no. 1 (1990): 23–27. http://dx.doi.org/10.1042/cs0790023.

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1. The aim of this work was to contribute to a better understanding of the mechanism by which Li+ administration impairs renal tubular acidification. 2. The kinetics of tubular acidification in the mid-proximal and distal convoluted tubules were studied by measuring intratubular pH using Sb microelectrodes during stopped-flow microperfusion with Krebs-Ringer bicarbonate (30 mmol/l) buffer. Four groups of male Wistar rats were utilized in this study: control, control plus lithium (C + Li+; one intraperitoneal injection of LiCl of 4 mmol l−1 day−1 kg−1 for 4 days), acidotic and acidotic plus lithium (A+ Li+). 3. In C + Li+ rats, the half-time of acidification was significantly higher than in control rats (P < 0.01), in both the mid-proximal tubule (11.3 ± 0.34 vs 6.73 ± 0.22 s) and the distal convoluted tubule (17.5 ± 0.31 vs 11.5 ± 1.02 s), and net HCO3− reabsorption was lower in both the mid-proximal tubule and the distal convoluted tubule. The effects of Li+ on tubular acidification kinetics were similar in acidotic rats. 4. A net Na+ flux, as measured by the Gertz split-droplet method, was significantly decreased in the mid-proximal tubule (P < 0.01) in C + Li+ rats compared with control rats (2.14 ± 0.17 vs 4.07 ± 0.39 nmol s−1 cm−2). 5. The transepithelial potential difference in the distal convoluted tubule was significantly lower (P < 0.01) in C + Li+ rats than in control rats (–7.50 ± 1.50 vs −20.5 ± 1.12 mV). 6. These findings suggest that Li+ causes a reduction in the apical Na+ gradients in both tubular segments, thereby decreasing the favourable driving force for H+ secretion.
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Schmitt, Roland, David H. Ellison, Nicolette Farman, et al. "Developmental expression of sodium entry pathways in rat nephron." American Journal of Physiology-Renal Physiology 276, no. 3 (1999): F367—F381. http://dx.doi.org/10.1152/ajprenal.1999.276.3.f367.

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During the past several years, sites of expression of ion transport proteins in tubules from adult kidneys have been described and correlated with functional properties. Less information is available concerning sites of expression during tubule morphogenesis, although such expression patterns may be crucial to renal development. In the current studies, patterns of renal axial differentiation were defined by mapping the expression of sodium transport pathways during nephrogenesis in the rat. Combined in situ hybridization and immunohistochemistry were used to localize the Na-Pi cotransporter type 2 (NaPi2), the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), the thiazide-sensitive Na-Cl cotransporter (NCC), the Na/Ca exchanger (NaCa), the epithelial sodium channel (rENaC), and 11β-hydroxysteroid dehydrogenase (11HSD). The onset of expression of these proteins began in post-S-shape stages. NKCC2 was initially expressed at the macula densa region and later extended into the nascent ascending limb of the loop of Henle (TAL), whereas differentiation of the proximal tubular part of the loop of Henle showed a comparatively retarded onset when probed for NaPi2. The NCC was initially found at the distal end of the nascent distal convoluted tubule (DCT) and later extended toward the junction with the TAL. After a period of changing proportions, subsegmentation of the DCT into a proximal part expressing NCC alone and a distal part expressing NCC together with NaCa was evident. Strong coexpression of rENaC and 11HSD was observed in early nascent connecting tubule (CNT) and collecting ducts and later also in the distal portion of the DCT. Ontogeny of the expression of NCC, NaCa, 11HSD, and rENaC in the late distal convolutions indicates a heterogenous origin of the CNT. These data present a detailed analysis of the relations between the anatomic differentiation of the developing renal tubule and the expression of tubular transport proteins.
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Cessac-Guillemet, A. L., F. Mounier, C. Borot, et al. "Characterization and distribution of albumin binding protein in normal rat kidney." American Journal of Physiology-Renal Physiology 271, no. 1 (1996): F101—F107. http://dx.doi.org/10.1152/ajprenal.1996.271.1.f101.

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The mechanism by which proteins that pass through the glomerular basal lamina are taken up by proximal tubule cells is incompletely characterized. Past work has identified the kinetics of albumin binding to renal brush-border membrane. We have now purified and characterized albumin binding protein (ABP) and shown its distribution in renal proximal tubular cells. ABP was purified from rat renal proximal tubular cell brush-border membrane by affinity chromatography with rat serum albumin-Sepharose. The resulting ABP had two apparent molecular masses (55 and 31 kDa) by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Antibodies to ABP were raised in rabbits and checked by immunoassay and immunoblotting. Light-microscopic immunohistochemistry showed ABP all along the proximal tubule in the pars convoluta and pars recta. Electron-microscopic immunohistochemistry showed labeling on microvilli and in apical endocytic vacuoles, dense apical tubules, and lysosomes. These results indicate that ABP is involved in proximal tubule endocytosis.
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Dominguez, J. H., M. Juhaszova, S. B. Kleiboeker, C. C. Hale, and H. A. Feister. "Na(+)-Ca2+ exchanger of rat proximal tubule: gene expression and subcellular localization." American Journal of Physiology-Renal Physiology 263, no. 5 (1992): F945—F950. http://dx.doi.org/10.1152/ajprenal.1992.263.5.f945.

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The activity of the Na(+)-Ca2+ exchanger, a membrane transporter that mediates Ca2+ efflux, has been described in amphibian and mammalian renal proximal tubules. However, demonstration of cell-specific expression of the Na(+)-Ca2+ exchanger in proximal renal tubules has been restricted to functional assays. In this work, Na(+)-Ca2+ exchanger gene expression in rat proximal tubules was characterized by three additional criteria: functional assay of transport activity in membrane vesicles derived from proximal tubules, expression of specific Na(+)-Ca2+ exchanger protein detected on Western blots, and determination of specific mRNA encoding Na(+)-Ca2+ exchanger protein on Northern blots. A new transport activity assay showed that proximal tubule membranes contained the highest Na(+)-Ca2+ exchanger transport activity reported in renal tissues. In dog renal proximal tubules and sarcolemma, a specific protein of approximately 70 kDa was detected, whereas in rat proximal tubules and sarcolemma, the specific protein approximated 65 kDa and was localized to the basolateral membrane. On Northern blots, a single 7-kb transcript isolated from rat proximal tubules, whole kidney, and heart hybridized under high-stringency conditions with rat heart cDNA. These data indicate that Na(+)-Ca2+ exchanger protein expressed in rat proximal tubule is similar, if not identical, to the cardiac protein. We suggest that the tubular Na(+)-Ca2+ exchanger characterized herein represents the Na(+)-Ca2+ exchanger described in functional assays of renal proximal tubules.
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Dissertations / Theses on the topic "Tubule renal"

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Bunt, Stephanie Marie. "Renal tubule morphogenesis in Drosophila." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612231.

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SILBER, PAUL MICHAEL. "EARLY INDICATION AND PATHOGENESIS OF RENAL PROXIMAL TUBULE INJURY (ENZYMURIA)." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184097.

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It is well known that a variety of toxicants can cause damage to the renal proximal tubule. However, the early pathogenesis of these deleterious interactions between a toxicant and this region of the nephron remain poorly understood. Thus, the purpose of this research was to attempt to answer three interrelated questions. First, what are the earliest changes in kidney function and structure after administration of tubule toxicants in vivo? Secondly, how do these structural/functional alterations change over time? Finally, are certain indicators of renal "dysfunction" more sensitive then others to the early stages of proximal tubule injury? The basic experimental approach consisted of injecting laboratory animals with a selective proximal tubule toxicant, and then collecting blood and/or urine at several timepoints after dosing; a variety of renal function indicators were evaluated at each of these timepoints. These included blood urea nitrogen (BUN), the glomerular filtration rate (GFR), and the excretion of glucose, protein, salts, glutathione, enzymes, and other endogenous molecules into the urine. At the termination of the exposure period the kidneys were evaluated histopathologically, and were also assayed for levels of specific enzymes and glutathione. Enzyme histochemistry was used to visualize changes in renal enzyme distribution, and protein electrophoretic methods permitted quantification of urinary proteins. These studies showed that specific markers of renal dysfunction were more sensitive to acute proximal tubule injury than other indicators. Specifically, the urinary excretion of proteins and the brush border membrane marker γ-glutamyl transpeptidase (GGT) were the best indicators of proximal tubule injury. Glucosuria, lysozymuria, and glutathionuria were all less sensitive markers, and changes in BUN or GFR were the poorest indicators of acute proximal tubule injury. These results indicated that the brush border membrane is one of the most susceptible regions of the proximal tubule to acute renal injury. Analysis of urinary protein electrophoresis patterns and kidney histopathology confirmed this hypothesis. This research also demonstrated the progression of the toxicant-tubule interaction over time, and showed that both tubule structure and function may be altered within minutes of administering a nephro-toxicant.
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Hunter, Robert William. "The renal distal convoluted tubule in apparent mineralocorticoid excess." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/17277.

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Lack of the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) causes the syndrome of apparent mineralocorticoid excess (AME): low-renin hypertension, renal sodium (Na +) retention, hypokalaemic alkalosis and polyuria. This rare autosomal recessive disorder is observed in human kindreds carrying mutations in the HSD11B2 gene. Genetically modified mice, in which the homologue Hsd11b2 is rendered non-functional, have been used to study the pathogenesis of AME. Hitherto, data obtained from humans and mice have suggested that the physiological phenotype is a consequence of enhanced reabsorption of Na + through the epithelial sodium channel (ENaC) in the renal connecting tubule (CNT) and collecting duct. However, Hsd11b2 null mice exhibit epithelial hypertrophy in a different nephron segment, namely the distal convoluted tubule (DCT). The studies described herein aimed to characterise this structural phenotype and to examine the consequences for renal Na + reabsorption in AME. Hsd11b2 null mice exhibited hypertrophy and hyperplasia in the DCT, with an elevated rate of epithelial cell proliferation in this nephron segment at 60 days of age. Hsd11b2 null kidneys contained greater quantities of the thiazide-sensitive NaCl co-transporter (NCC), the dominant Na + transporter protein in the DCT. They also contained greater quantities of the phosphorylated forms of NCC that are associated with NaCl transport activity. Despite this, there was no increase in the proportion of filtered Na + that was reabsorbed in the DCT. This was assessed in anaesthetised mice, using clearance methodology to measure the thiazide-induced increment in the fractional excretion of Na + (FENa) during continuous ENaC blockade. Wild-type DCTs did not express 11βHSD2; therefore the structural and molecular changes were not a direct consequence of the loss of 11βHSD2 in affected cells. The discussion examines the likely mechanisms causing structural remodelling in the distal renal tubule of Hsd11b2 null kidneys and potential explanations for the dissociation between structural and functional phenotypes in the DCT. There are implications for our understanding of the cellular and molecular mechanisms underlying various renal phenomena including structural remodelling in the distal tubule, resolution of the ‘aldosterone paradox’ and escape from chronic aldosterone excess.
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White, S. J. "Anion transport in the renal proximal tubule of the rat." Thesis, University of Manchester, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376286.

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Takaori, Koji. "Severity and Frequency of Proximal Tubule Injury Determines Renal Prognosis." Kyoto University, 2018. http://hdl.handle.net/2433/232126.

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Vekaria, Renu. "The functional role of extracellular nucleotides in the renal tubule." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1446143/.

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There is increasing evidence that extracellular nucleotides (such as ATP, ADP, UTP and UDP), as well as the nucleoside adenosine, behave as autocrine or paracrine agents in most tissues including the kidney, acting on a group of receptors known as purinoceptors. Previous studies have shown that activation of these receptors by exogenous nucleotides can influence a variety of renal vascular and tubular functions. Purinoceptors of various subtypes are present on basolateral and apical membranes of renal tubules. However, the extent to which apical receptors are stimulated by endogenous nucleotides is unknown. Using micropuncture, the first part of this study quantified endogenous ATP in the lumen of proximal and distal tubules of the rat in vivo, both under control conditions and during pathophysiological manoeuvres. The results showed that ATP levels were sufficiently high to activate some purinoceptor subtypes. To assess whether the intraluminal ATP was being secreted or merely filtered at the glomerulus, the ATP content of fluid from Bowman's space (in Munich-Wistar rats) was compared with that in proximal tubules. The conclusion was that tubular epithelial cells secrete ATP. Using a proximal tubular epithelial cell line, the mechanism of ATP release was examined. Intracellular stores of ATP were visualised using a marker compound (quinacrine), and the fate of these stores was monitored following hypotonic stimulation of ATP release. The findings suggested that ATP is stored within the cytoplasm, possibly in vesicles, and is released by exocytosis. In the final part of the investigation, using immunohistochemistry, the distribution of five nucleotide-hydrolysing ectonucleotidases, namely NTPDases 1-3, NPP3 and ecto-5'- nucleotidase, was examined along the rat nephron. These enzymes (which differ in their hydrolysis pathways) were found to be differentially expressed along the major segments of the nephron, suggesting that they may be strategically located to influence the activity of the different purinoceptor subtypes.
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Selbi, Wisam Dhafer Rashid. "Regulation and function of hyaluronan in renal proximal tubule epithelial cells." Thesis, Cardiff University, 2006. http://orca.cf.ac.uk/54266/.

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v. HA binding proteins (Hyaladherins) differentially affected extracellular HA structures. Inter-alpha-trypsin inhibitor (loci) is important in the formation of HA coats as well as HA cables. Tumour necrosis factor-stimulated gene-6 (TSG-6) is seen to be crucial to the formation of HA coats but not HA cables, while the role of versican in either structures is not fully determined yet although it is thought to be more crucial to the formation of HA cables.
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Shah, Nileshkumar. "Expression and regulation of cadherin of human renal proximal tubule epithelial cells." Thesis, St George's, University of London, 2018. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.754076.

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Cadherins are a family of trans-membrane junctional proteins important in maintenance of cell-cell junction, phenotype regulation, tissue organisation and embryonic development. The proteins form calcium dependent homophilic cell junctional complexes and bind internally to the actin cytoskeleton and regulate intracellular signalling via the p- catenin pathway. Altered cadherin expression is essential for embryonic development, tissue repair or healing, fibrosis, cancer and metastasis. Much interest has developed in cadherin expression and its regulation along with signalling in renal proximal tubule epithelial cells (PTECs), an important cell type in the development of tubulointerstitial fibrosis and a potential source of myofibroblasts.
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Frohlich, Else Marie. "A microphysiological in vitro model of the renal proximal tubule reabsorptive barrier." Thesis, Boston University, 2014. https://hdl.handle.net/2144/12102.

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Thesis (Ph.D.)--Boston University
Microfabricated in vitro kidney tissue models replicate essential components of in vivo kidney physiology, providing a platform for direct observation of controlled yet physiologically-representative kidney tissue. Currently, static and flat cell culture environments serve as platforms to study cell behavior, tissue structure formation, renal disease mechanisms, and drug development. Petri dishes, well plates, and flasks sustain cell growth, but their environments lacks physiological cues that are present in the in vivo environment, prompting cell responses that may not be physiologically-representative. One alternative to these flat, static environments is to use animal models, which offer an in vivo environment but inherently come with uncontrollable fluctuations that introduce variables into the test setting. Microfabricated kidney tissue models improve upon other in vitro kidney tissue models by precisely controlling the geometry of device components via high-resolution fabrication and forming processes. Control over device component geometry consequently dictates control over mechanical parameters which influence and guide kidney cell and tissue structure and function. In addition, microfabrication methods create platforms compatible with the various cells, materials, and chemistries which also provide cues leading to replication of critical kidney function in vitro. The objective of this work is to develop an in vitro model of kidney tissue with physiologically-accurate replication of renal proximal tubule function. In chapter one, we have established a microphysiological model system of renal proximal tubule epithelia by a) characterizing the effect of user-defined physiological parameters on renal proximal tubule cells, and b) incorporating those parameters into a bilayer microfluidic device to model the renal reabsorptive barrier. In chapter two, we have characterized function o f our renal tissue model to establish metrics o f kidney-specific function , including reabsorption. In chapter three, we extend our proximal tubule model to include microvascular endothelial tissue and applied the metrics established in chapter 2 to quantify reabsorptive barrier function in the coculture model. This microphysiological model system provides an in vitro platform on which to model reabsorptive tissue barriers with kidney-specific function which enables meaningful applications for understanding biological transport phenomenon, observing underlying disease mechanisms, and improving the drug discovery process.
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Marable, Sierra S. "The Role of Hepatocyte Nuclear Factor 4a in Renal Proximal Tubule Development." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1595849621045508.

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Books on the topic "Tubule renal"

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Jones, Caroline Elizabeth Mary. The development, evaluation and use of freshly isolated renal proxinal tubule systems in the fischer rat. Aston University. Department of Pharmaceutical Sciences, 1990.

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Parker, James N., and Philip M. Parker. The Official patient's sourcebook on renal tubular acidosis. Icon Health Publications, 2002.

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Najjar, Samer. Effects of ischemia and reperfusion on mitochondrial phosphate uptake in rat renal proximal tubules. s.n.], 1993.

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Wong, P. S. K. The use of NMR spectroscopy to follow intracellular sodium content in rat rental proximal tubules. University of Birmingham, 1994.

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Tamagno, Jose. Hypervelocity real gas capabilities of GASL's expansion tube (HYPULSE) facility. American Institute of Aeronautics and Astronautics, 1990.

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Byrne, Kevin Michael. Real-time modeling of cross-body flow for torpedo tube recovery of the Phoenix Autonomous Underwater Vehicle (AUV). Naval Postgraduate School, 1998.

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Wagner, Carsten A., and Olivier Devuyst. Renal acid–base homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0024.

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The kidney is central to acid–base homeostasis. Major processes are reabsorption of filtered bicarbonate, de novo synthesis of bicarbonate from ammoniagenesis, and net excretion of protons. The latter requires buffers such as ammonium, phosphate, citrate and other bases binding protons (so-called titratable acids). The proximal tubule is the major site of bicarbonate reabsorption and only site of ammoniagenesis. The thick ascending limb and the distal convoluted tubule handle ammonia/ammonium and complete bicarbonate reabsorption. The collecting duct system excretes protons and ammonium, but may switch to net bicarbonate secretion. The kidney displays a great plasticity to adapt acid or bicarbonate excretion. Angiotensin II, aldosterone and endothelin are involved in regulating these processes, and they induce morphological changes along the nephron. Inborn and acquired disorders of renal acid–base handling are caused by mutations in acid–base transport proteins or by dysregulation of adaptive mechanisms.
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Speeckaert, Marijn, and Joris Delanghe. Tubular function. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0008.

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Assessment of tubular function is more complicated than the measurement of glomerular filtration rate. Different functions may be affecting according to the different segments of tubule involved. Key tests include concentrating and diluting capacity, and fractional excretion of sodium. Tubular proteinuria occurs when glomerular function is normal, but when the proximal tubules have a diminished capacity to reabsorb and to catabolize proteins, causing an increased urinary excretion of the low-molecular-mass proteins that normally pass through the glomerulus. Proximal tubular dysfunction is characterized by hypophosphataemia, and a variety of other abnormalities characteristics of the renal Fanconi syndrome. Distinguishing the location of the lesion in Renal Tubular Acidosis is considered in Chapter 35.
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Houillier, Pascal. Magnesium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0027.

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Magnesium is critically important in the process of energy release. Although most magnesium is stored outside the extracellular fluid compartment, the regulated concentration appears in blood. Urinary magnesium excretion can decrease rapidly to low values when magnesium entry rate into the extracellular fluid volume is low, which has several important implications: cell and bone magnesium do not play a major role in the defence of blood magnesium concentration; while a major role is played by the kidney and especially the renal tubule, which adapts to match the urinary magnesium excretion and net entry of magnesium into extracellular fluid. In the kidney, magnesium is reabsorbed in the proximal tubule, the thick ascending limb of the loop of Henle (TALH), and the distal convoluted tubule (DCT). Magnesium absorption is mainly paracellular in the proximal tubule and TALH, whereas it is transcellular in the DCT. The hormone(s) regulating renal magnesium transport and blood magnesium concentration are not fully understood. Renal tubular magnesium transport is altered by a number of hormones, mainly in the TALH and DCT. Parathyroid hormone, calcitonin, arginine vasopressin, ß-adrenergic agonists, and epidermal growth factor, all increase renal tubular magnesium reabsorption; in contrast, prostaglandin E2 decreases magnesium reabsorption. Non-hormonal factors also influence magnesium reabsorption: it is decreased by high blood concentrations of calcium and magnesium, probably via the action of divalent cations on the calcium-sensing receptor; metabolic acidosis decreases, and metabolic alkalosis increases, renal magnesium reabsorption.
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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 proximal renal tubule epithelium. A further 5%–10% of renal cancers are transitional cell (urothelial) carcinomas of the renal pelvis. Benign kidney tumours, such as cysts, are also common.
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Book chapters on the topic "Tubule renal"

1

Lote, Christopher J. "The Proximal Tubule." In Principles of Renal Physiology. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3785-7_5.

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2

Lote, Christopher J. "The proximal tubule." In Principles of Renal Physiology. Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-6470-2_5.

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3

Lote, Chris. "The proximal tubule." In Principles of Renal Physiology. Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4086-7_5.

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4

Pavelka, Margit, and Jürgen Roth. "Renal Proximal Tubule: A Reabsorption Plant." In Functional Ultrastructure. Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_118.

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Terryn, Sara, and Olivier Devuyst. "Oxidative Stress in the Kidney: Proximal Tubule Disorders." In Studies on Renal Disorders. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-857-7_10.

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6

Lote, Christopher J. "The Loop of Henle, Distal Tubule and Collecting Duct." In Principles of Renal Physiology. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3785-7_6.

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7

Lote, Christopher J. "The loop of Henle, distal tubule and collecting duct." In Principles of Renal Physiology. Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-6470-2_6.

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8

Lote, Chris. "The loop of Henle, distal tubule and collecting duct." In Principles of Renal Physiology. Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4086-7_6.

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9

Foo, Suan East, Anirban Kundu, Hwee Ying Lim, Kim Ping Wong, and Partha Roy. "Directed Transport in Renal Proximal Tubule Cells." In IFMBE Proceedings. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14515-5_190.

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10

Weinstein, Alan M. "Assessing Homeostatic Properties of Epithelial Cell Models: Application to Kidney Proximal Tubule." In Membrane Transport and Renal Physiology. Springer New York, 2002. http://dx.doi.org/10.1007/978-1-4684-9252-1_7.

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Conference papers on the topic "Tubule renal"

1

Topletz-Erickson, Ariel R., Anthony Lee, JoAl Mayor, et al. "Abstract 3015: Tucatinib inhibits creatinine and metformin renal tubule secretion but has no effect on renal function (GFR)." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3015.

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2

Heller, Daniel A., Edgar Jaimes, Ryan Williams, and Janki Shah. "Abstract 2032: Renal tubule-targeted supportive care nanotherapy for cisplatin-induced acute kidney injury." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2032.

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3

Taub, Mary L., and Sunil Sudarshan. "Abstract 4364: Oncometabolite L-2-hydroxyglutarate blocks differentiation of renal proximal tubule cells in matrigel." 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.sabcs18-4364.

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Taub, Mary L., and Sunil Sudarshan. "Abstract 4364: Oncometabolite L-2-hydroxyglutarate blocks differentiation of renal proximal tubule cells in matrigel." 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.am2019-4364.

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5

Wyman, Aaron J., and Mary Alice Webb. "Calcium Oxalate Accumulation in Malpighian Tubules of Silkworm (Bombyx mori)." In RENAL STONE DISEASE: 1st Annual International Urolithiasis Research Symposium. AIP, 2007. http://dx.doi.org/10.1063/1.2723606.

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Verkoelen, Carl F. "Hyaluronan in Tubular and Interstitial Nephrocalcinosis." In RENAL STONE DISEASE: 1st Annual International Urolithiasis Research Symposium. AIP, 2007. http://dx.doi.org/10.1063/1.2723560.

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Moe, Orson W., Daniel G. Fuster, Xiao-Song Xie, et al. "Distal Renal Tubular Acidosis and Calcium Nephrolithiasis." In RENAL STONE DISEASE 2: 2nd International Urolithiasis Research Symposium. AIP, 2008. http://dx.doi.org/10.1063/1.2998065.

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8

Westwood, Brian M., Hossam A. Shaltout, and Mark C. Chappell. "Modeling of Angiotensin Peptide Metabolism in Renal Proximal Tubules." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-190990.

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The recent discovery of angiotensin converting enzyme 2 (ACE2) as a functional peptidase within the renin-angiotensin system (RAS) has added a new layer of complexity to the enzymatic cascade of this hormonal system. ACE2 is highly expressed in the proximal tubules of the kidney, an important tissue site involved in blood pressure regulation. Therefore, we derived a model for the processing of Ang I which is the immediate precursor to the biologically active peptides Ang II and Ang-(1-7) based on metabolism data in isolated proximal tubules of the sheep kidney (1). Given the individual experimental velocities for several peptidases expressed in the proximal tubules including ACE, ACE2 and neprilysin, rate constants were calculated to describe the conservation equations for the processing of Ang I, Ang II and Ang-(1-7) We modeled the system with Ang I as the initial substrate and peptide concentrations for the downstream products were calculated using Euler’s method.
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Sohrabi, Salman, Seyyed Mahdi Nemati Mehr, and Pedram Falsafi. "A Novel Approach for Compensating the Significance of Tubule’s Architecture in Urine Concentrating Mechanism of Renal Medulla." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-63747.

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Many theories and mathematical simulations have been proposed concerning urine concentrating mechanism (UCM). The WKM and region approach are the two most valuable methods for compensating the effect of tubule’s architecture in renal medulla. They both have tried to simulate tubule’s confinement within a particular region mathematically in one spatial dimension. In this study, continuity, momentum and species transport equations along with standard expressions for transtubular solutes and water transports on tubule’s membrane were solved numerically in three spatial dimensions which practically is the main significance of our novel approach. Model structure has been chosen as simple as possible to minimize the effect of other factors in tubule’s solute and water exchange. It has been tried to simulate the preferential interaction between tubules by introducing different diffusion coefficients for solutes in the intermediate media in order that changing this physical parameter directly could influence tubule’s confinement with respect to each other. The results have been discussed in detail and then the effect of solute’s diffusivity on UCM has been investigated subsequently. In overall, it has been found out that this simulation can validate the integrity of our proposed approach for further investigation in this field.
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Hu, Dong, and Zheng Baoyu. "Joint segmentation scheme for renal tubular image." In Second International Conference on Image and Graphics, edited by Wei Sui. SPIE, 2002. http://dx.doi.org/10.1117/12.477165.

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