Academic literature on the topic 'Tubule-T'

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Journal articles on the topic "Tubule-T"

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Frisk, Michael, Jussi T. Koivumäki, Per A. Norseng, Mary M. Maleckar, Ole M. Sejersted, and William E. Louch. "Variable t-tubule organization and Ca2+ homeostasis across the atria." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 4 (August 15, 2014): H609—H620. http://dx.doi.org/10.1152/ajpheart.00295.2014.

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Although t-tubules have traditionally been thought to be absent in atrial cardiomyocytes, recent studies have suggested that t-tubules exist in the atria of large mammals. However, it is unclear whether regional differences in t-tubule organization exist that define cardiomyocyte function across the atria. We sought to investigate regional t-tubule density in pig and rat atria and the consequences for cardiomyocyte Ca2+ homeostasis. We observed t-tubules in approximately one-third of rat atrial cardiomyocytes, in both tissue cryosections and isolated cardiomyocytes. In a minority (≈10%) of atrial cardiomyocytes, the t-tubular network was well organized, with a transverse structure resembling that of ventricular cardiomyocytes. In both rat and pig atrial tissue, we observed higher t-tubule density in the epicardium than in the endocardium. Consistent with high variability in the distribution of t-tubules and Ca2+ channels among cells, L-type Ca2+ current amplitude was also highly variable and steeply dependent on capacitance and t-tubule density. Accordingly, Ca2+ transients showed great variability in Ca2+ release synchrony. Simultaneous imaging of the cell membrane and Ca2+ transients confirmed t-tubule functionality. Results from mathematical modeling indicated that a transmural gradient in t-tubule organization and Ca2+ release kinetics supports synchronization of contraction across the atrial wall and may underlie transmural differences in the refractory period. In conclusion, our results indicate that t-tubule density is highly variable across the atria. We propose that higher t-tubule density in cells localized in the epicardium may promote synchronization of contraction across the atrial wall.
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Kong, Cherrie H. T., Eva A. Rog-Zielinska, Peter Kohl, Clive H. Orchard, and Mark B. Cannell. "Solute movement in the t-tubule system of rabbit and mouse cardiomyocytes." Proceedings of the National Academy of Sciences 115, no. 30 (July 10, 2018): E7073—E7080. http://dx.doi.org/10.1073/pnas.1805979115.

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Cardiac transverse (t-) tubules carry both electrical excitation and solutes toward the cell center but their ability to transport small molecules is unclear. While fluorescence recovery after photobleaching (FRAP) can provide an approach to measure local solute movement, extraction of diffusion coefficients is confounded by cell and illumination beam geometries. In this study, we use measured cellular geometry and detailed computer modeling to derive the apparent diffusion coefficient of a 1-kDa solute inside the t-tubular system of rabbit and mouse ventricular cardiomyocytes. This approach shows that diffusion within individual t-tubules is more rapid than previously reported. T-tubule tortuosity, varicosities, and the presence of longitudinal elements combine to substantially reduce the apparent rate of solute movement. In steady state, large (>4 kDa) solutes did not freely fill the t-tubule lumen of both species and <50% of the t-tubule volume was available to solutes >70 kDa. Detailed model fitting of FRAP data suggests that solute diffusion is additionally restricted at the t-tubular entrance and this effect was larger in mouse than in rabbit. The possible structural basis of this effect was investigated using electron microscopy and tomography. Near the cell surface, mouse t-tubules are more tortuous and filled with an electron-dense ground substance, previously identified as glycocalyx and a polyanionic mesh. Solute movement in the t-tubule network of rabbit and mouse appears to be explained by their different geometric properties, which impacts the use of these species for understanding t-tubule function and the consequences of changes associated with t-tubule disease.
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Uchida, Keita, Azadeh Nikouee, Greta Tamkus, and Anatoli N. Lopatin. "T-Tubular Constrictions Promote T-Tubule Sealing." Biophysical Journal 114, no. 3 (February 2018): 619a. http://dx.doi.org/10.1016/j.bpj.2017.11.3349.

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Bryant, Simon M., Cherrie H. T. Kong, Judy J. Watson, Hanne C. Gadeberg, David M. Roth, Hemal H. Patel, Mark B. Cannell, Andrew F. James, and Clive H. Orchard. "Caveolin-3 KO disrupts t-tubule structure and decreases t-tubular ICa density in mouse ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 5 (November 1, 2018): H1101—H1111. http://dx.doi.org/10.1152/ajpheart.00209.2018.

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Caveolin-3 (Cav-3) is a protein that has been implicated in t-tubule formation and function in cardiac ventricular myocytes. In cardiac hypertrophy and failure, Cav-3 expression decreases, t-tubule structure is disrupted, and excitation-contraction coupling is impaired. However, the extent to which the decrease in Cav-3 expression underlies these changes is unclear. We therefore investigated the structure and function of myocytes isolated from the hearts of Cav-3 knockout (KO) mice. These mice showed cardiac dilatation and decreased ejection fraction in vivo compared with wild-type control mice. Isolated KO myocytes showed cellular hypertrophy, altered t-tubule structure, and decreased L-type Ca2+ channel current ( ICa) density. This decrease in density occurred predominantly in the t-tubules, with no change in total ICa, and was therefore a consequence of the increase in membrane area. Cav-3 KO had no effect on L-type Ca2+ channel expression, and C3SD peptide, which mimics the scaffolding domain of Cav-3, had no effect on ICa in KO myocytes. However, inhibition of PKA using H-89 decreased ICa at the surface and t-tubule membranes in both KO and wild-type myocytes. Cav-3 KO had no significant effect on Na+/Ca2+ exchanger current or Ca2+ release. These data suggest that Cav-3 KO causes cellular hypertrophy, thereby decreasing t-tubular ICa density. NEW & NOTEWORTHY Caveolin-3 (Cav-3) is a protein that inhibits hypertrophic pathways, has been implicated in the formation and function of cardiac t-tubules, and shows decreased expression in heart failure. This study demonstrates that Cav-3 knockout mice show cardiac dysfunction in vivo, while isolated ventricular myocytes show cellular hypertrophy, changes in t-tubule structure, and decreased t-tubular L-type Ca2+ current density, suggesting that decreased Cav-3 expression contributes to these changes in cardiac hypertrophy and failure.
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Hong, TingTing, and Robin M. Shaw. "Cardiac T-Tubule Microanatomy and Function." Physiological Reviews 97, no. 1 (January 2017): 227–52. http://dx.doi.org/10.1152/physrev.00037.2015.

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Unique to striated muscle cells, transverse tubules (t-tubules) are membrane organelles that consist of sarcolemma penetrating into the myocyte interior, forming a highly branched and interconnected network. Mature t-tubule networks are found in mammalian ventricular cardiomyocytes, with the transverse components of t-tubules occurring near sarcomeric z-discs. Cardiac t-tubules contain membrane microdomains enriched with ion channels and signaling molecules. The microdomains serve as key signaling hubs in regulation of cardiomyocyte function. Dyad microdomains formed at the junctional contact between t-tubule membrane and neighboring sarcoplasmic reticulum are critical in calcium signaling and excitation-contraction coupling necessary for beat-to-beat heart contraction. In this review, we provide an overview of the current knowledge in gross morphology and structure, membrane and protein composition, and function of the cardiac t-tubule network. We also review in detail current knowledge on the formation of functional membrane subdomains within t-tubules, with a particular focus on the cardiac dyad microdomain. Lastly, we discuss the dynamic nature of t-tubules including membrane turnover, trafficking of transmembrane proteins, and the life cycles of membrane subdomains such as the cardiac BIN1-microdomain, as well as t-tubule remodeling and alteration in diseased hearts. Understanding cardiac t-tubule biology in normal and failing hearts is providing novel diagnostic and therapeutic opportunities to better treat patients with failing hearts.
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Uchida, Keita, Ian Moench, Greta Tamkus, and Anatoli N. Lopatin. "Small membrane permeable molecules protect against osmotically induced sealing of t-tubules in mouse ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 311, no. 1 (July 1, 2016): H229—H238. http://dx.doi.org/10.1152/ajpheart.00836.2015.

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Cardiac t-tubules are critical for efficient excitation-contraction coupling but become significantly remodeled during various stress conditions. However, the mechanisms by which t-tubule remodeling occur are poorly understood. Recently, we demonstrated that recovery of mouse ventricular myocytes after hyposmotic shock is associated with t-tubule sealing. In this study, we found that the application of Small Membrane Permeable Molecules (SMPM) such as DMSO, formamide and acetamide upon washout of hyposmotic solution significantly reduced the amount of extracellular dextran trapped within sealed t-tubules. The SMPM protection displayed sharp biphasic concentration dependence that peaks at ∼140 mM leading to >3- to 4-fold reduction in dextran trapping. Consistent with these data, detailed analysis of the effects of DMSO showed that the magnitude of normalized inward rectifier tail current ( IK1,tail), an electrophysiological marker of t-tubular integrity, was increased ∼2-fold when hyposmotic stress was removed in the presence of 1% DMSO (∼140 mM). Analysis of dynamics of cardiomyocytes shrinking during resolution of hyposmotic stress revealed only minor increase in shrinking rate in the presence of 1% DMSO, and cell dimensions returned fully to prestress values in both control and DMSO groups. Application and withdrawal of 10% DMSO in the absence of preceding hyposmotic shock induced classical t-tubule sealing. This suggests that the biphasic concentration dependence originated from an increase in secondary t-tubule sealing when high SMPM concentrations are removed. Overall, the data suggest that SMPM protect against sealing of t-tubules following hyposmotic stress, likely through membrane modification and essentially independent of their osmotic effects.
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Orchard, Clive. "T-tubule trouble." Journal of Physiology 574, no. 2 (July 6, 2006): 330. http://dx.doi.org/10.1113/jphysiol.2006.113803.

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Chung, Ka Young, Misuk Kang, and Jeffery W. Walker. "Contractile regulation by overexpressed ETArequires intact T tubules in adult rat ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (May 2008): H2391—H2399. http://dx.doi.org/10.1152/ajpheart.00011.2008.

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Endothelin (ET)-1 regulates the contractility and growth of the heart by binding G protein-coupled receptors of the ET type A receptor (ETA)/ET type B (ETB) receptor family. ETA, the predominant ET-1 receptor subtype in myocardium, is thought to localize preferentially within cardiac T tubules, but the consequences of mislocalization are not fully understood. Here we examined the effects of the overexpression of ETAin conjunction with T-tubule loss in cultured adult rat ventricular myocytes. In adult myocytes cultured for 3 to 4 days, the normally robust positive inotropic effect (PIE) of ET-1 was lost in parallel with T-tubule degeneration and a decline in ETAprotein levels. In these T tubule-compromised myocytes, an overexpression of ETAusing an adenoviral vector did not rescue the responsiveness to ET-1, despite the robust expression in the surface sarcolemma. The inclusion of the actin polymerization inhibitor cytochalasin D (CD) during culture prevented gross morphological changes including a loss of T tubules and a rounding of intercalated discs, but CD alone did not rescue the responsiveness to ET-1 or prevent ETAdownregulation. The rescue of a normal PIE in 3- to 4-day cultured myocytes required both an increased expression of ETAand intact T tubules (preserved with CD). Therefore, the activation of ETAlocalized in T tubules was associated with a strong PIE, whereas the activation of ETAin surface sarcolemma was not. The results provide insight into the pathological cardiac conditions in which ETAis upregulated and T-tubule morphology is altered.
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Jayasinghe, Isuru D., Alexander H. Clowsley, Michelle Munro, Yufeng Hou, David J. Crossman, and Christian Soeller. "Revealing t-tubules in striated muscle with new optical super-resolution microscopy techniques." European Journal of Translational Myology 25, no. 1 (December 24, 2014): 15. http://dx.doi.org/10.4081/ejtm.2015.4747.

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The t-tubular system plays a central role in the synchronisation of calcium signalling and excitation-contraction coupling in most striated muscle cells. Light microscopy has been used for imaging t-tubules for well over 100 years and together with electron microscopy (EM), has revealed the three-dimensional complexities of the t-system topology within cardiomyocytes and skeletal muscle fibres from a range of species. The emerging super-resolution single molecule localisation microscopy (SMLM) techniques are offering a near 10-fold improvement over the resolution of conventional fluorescence light microscopy methods, with the ability to spectrally resolve nanometre scale distributions of multiple molecular targets. In conjunction with the next generation of electron microscopy, SMLM has allowed the visualisation and quantification of intricate t-tubule morphologies within large areas of muscle cells at an unprecedented level of detail. In this paper, we review recent advancements in the t-tubule structural biology with the utility of various microscopy techniques. We outline the technical considerations in adapting SMLM to study t-tubules and its potential to further our understanding of the molecular processes that underlie the sub-micron scale structural alterations observed in a range of muscle pathologies.
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Muñoz, P., M. Rosemblatt, X. Testar, M. Palacín, G. Thoidis, P. F. Pilch, and A. Zorzano. "The T-tubule is a cell-surface target for insulin-regulated recycling of membrane proteins in skeletal muscle." Biochemical Journal 312, no. 2 (December 1, 1995): 393–400. http://dx.doi.org/10.1042/bj3120393.

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(1) In this study we have determined the distribution of various membrane proteins involved in insulin-activated glucose transport in T-tubules and in sarcolemma from rat skeletal muscle. Two independent experimental approaches were used to determine the presence of membrane proteins in T-tubules: (i) the purification of T-tubules free from sarcolemmal membranes by lectin agglutination, and (ii) T-tubule vesicle immunoadsorption. These methods confirmed that T-tubules from rat skeletal muscle were enriched with dihydropyridine receptors and tt28 protein and did not contain the sarcolemmal markers dystrophin or beta 1-integrin. Both types of experiments revealed an abundant content of GLUT4 glucose carriers, insulin receptors and SCAMPs (secretory carrier membrane proteins) in T-tubule membranes. (2) Acute administration in vivo of insulin caused an increased abundance of GLUT4 in T-tubules and sarcolemma. On the contrary, insulin led to a 50% reduction in insulin receptors present in T-tubules and in sarcolemma, demonstrating that insulin-induced insulin receptor internalization affects T-tubules in the muscle fibre. The alteration in the content of GLUT4 and insulin receptors in T-tubules was a consequence of insulin-induced redistribution of these proteins. SCAMPs also redistributed in muscle membranes in response to insulin. They were recruited by insulin from intracellular high-density fractions to intracellular lighter-density fractions and to the cell surface, showing a pattern of insulin-induced cellular redistribution distinct from those of GLUT4 and the insulin receptor. (3) In conclusion, the T-tubule is a cell-surface target for membrane proteins involved in recycling such as SCAMPs or for membrane proteins that acutely redistribute in response to insulin such as GLUT4 or insulin receptors.
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Dissertations / Theses on the topic "Tubule-T"

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Deshpande, A. M. "Structure-function analysis of the role of amphiphysin in T-tubule organisation in Drosophila." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598514.

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To investigate how amphiphysin contributes to T-tubule organisation in Drosophila, I initiated a structure-function analysis of the protein in this process. I assayed the ability of different domains and mutant forms of the protein to rescue the amphiphysin null mutant phenotype. When either an N-terminal fragment that includes the BAR domain, or the SH3 domain, was expressed in an amphiphysin mutant background, there was no obvious rescue of the T-tubule defect. However, expression of full-length protein lacking the first 40 amino acids resulted in some rescue of reticular structures. When full-length amphiphysin, carrying a mutated SH3 domain that does not interact with praline-containing motifs, was expressed in amphiphysin mutants, tubular structures similar to those of wild type were seen, but they failed to localise normally. When full-length amphiphysin, carrying point mutations in the BAR domain that inhibit its binding and tabulating activity, was expressed in amphiphysin mutants, there was an partial rescue of the phenotype. Although amphiphysin is known to dimerise, neither an N-terminal region containing the BAR domain, nor the SH3 domain, had any detectable dominant negative phenotype in a wild type background. I also examined muscle development in embryos, to detect whether amphiphysin expression occurred before or after T-tubule formation. I examined the time course of amphiphysin and Dig (another T-tubule marker) expression in developing muscles. Amphiphysin appeared first on the plasma membrane and as intracellular puncta, then on a reticular network, presumably T-tubules. Dig could be detected on T-tubules only subsequently to this. Therefore, amphiphysin expression in muscles precedes the earliest time at which T-tubules can be detected with any markers available to me.
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He, Yang. "Modelling the spatio-temporal dynamic of iIntracellular Ca2+ handling system in cardiac cells." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/modelling-the-spatiotemporal-dynamic-of-intracellular-ca2-handling-system-in-cardiac-cells(f1a1b52a-f9f1-4837-aa0f-9d5df1f54d6f).html.

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The intracellular Ca2+ handling system in a cardiac myocyte is of crucial importance. It regulates the contraction and relaxation of the myocyte during the excitation-contraction (EC) coupling. A normal intracellular Ca2+ handling system keeps the contraction of the heart orderly, which represents a powerful force to pump blood to the whole body. However, disarrayed or remodelled cellular structure associated with the intracellular Ca2+ handling system at the subcellular level, such as loss of T-tubule network in diseased conditions, may promote abnormal cardiac EC coupling, leading to genesis of cardiac arrhythmias impairing cardiac mechanical functions. Up to date, it is still incompletely understood how the intracellular Ca2+ handling system is altered by changes in subcellular structures of Ca2+ handling systems. In this thesis, biophysically detailed computational models for the intracellular Ca2+ handling system of a cardiac cell were developed, providing a powerful platform to investigate the spatio-temporal complexity associated with the intracellular Ca2+ handling, and its role in generating abnormal cardiac EC coupling. First, a well-validated single cell model was used to investigate how the diastolic and systolic Ca2+ concentration responded to alterations in the model parameters related to the Ca2+ handling system, from which the mechanisms underlying the rate-dependence of EC coupling were analysed. Then, a novel single cell model, with a 2D presentation of the spatial structures of subcellular Ca2+ handling and membrane action potential, of a sheep atrial myocyte was developed for simulating the abnormal intracellular Ca2+ regulation system due to the loss of T-tubules during atrial fibrillation. Variant scenarios of T-tubule loss were considered to investigate the role of the T-tubule in affecting the intracellular Ca2+ regulation. Furthermore, membrane currents' alterations due to the electrical remodelling arising from atrial fibrillation were considered together with the loss of T-tubule. Three typical types of abnormal Ca2+ cycling phenomenon, namely intracellular Ca2+ alternans, spontaneous Ca2+ sparks and intracellular Ca2+ waves were observed in AF conditions. The relationship between T-tubule loss, AF-remodelling and the genesis of delayed afterdepolarizations (DADs) was also investigated. It was shown that the loss of T-tubule in AF condition played an important role in disturbing the Ca2+ regulation system, which increases the risk for a cell to generate impaired contraction.
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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/independent mechanisms involving various immuno-regulatory molecules including PD-L1, sHLA-G and IDO. The overall outcome of this down-regulation is suppressed DC maturation, decreased number of antibody producing B cells and low T cell responses. These manifestations within a clinical setting are expected to dampen the ongoing inflammation, preventing the damage caused to the kidney tissue.
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Lemerle, Eline. "Rôle des cavéoles dans la formation des tubules-T et dans la physiopathologie des cavéolinopathies." Electronic Thesis or Diss., Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS010.pdf.

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Dans le muscle squelettique, des invaginations du sarcolemme appelées cavéoles et leur composant principal Cav-3 seraient impliqués dans la formation des tubules transverses, des structures musculaires permettant de propager le potentiel d'action dans la fibre musculaire. Pourtant, ce mécanisme demeure à ce jour inconnu. L’importance des cavéoles et de Cav-3 est accentuée par l’existence de défauts dans l’organisation et la fonction des cavéoles dans le cas de cavéolinopathies, des maladies neuromusculaires autosomiques dominantes dues à des mutations dans le gène CAV-3 et dont les mécanismes physiopathologiques sont à ce jour incompris. L’objectif de mon projet était de comprendre le rôle des cavéoles dans la formation précoce des tubules-T. Une technique de microscopie corrélative combinant de la fluorescence à super résolution et de la microscopie électronique sur répliques de métal a permis d’examiner en détails les composants moléculaires des cavéoles et des tubules-T dans des myotubes extensivement différenciés. J’ai ainsi montré l'organisation des cavéoles sur des plateformes de Bin1 formant ainsi une nouvelle structure en anneaux semblant optimiser la tubulation de la membrane afin d’initier la formation des tubules-T. Ces anneaux ainsi que la tubulation des membranes par Bin1 sont altérés dans le cas de défauts d’expression de Cav-3 et dans les myotubes de patients cavéolinopathes. Mes travaux suggèrent que les anneaux de cavéoles constituent le site d’initiation des tubules-T et apportent les bases d’une caractérisation de la biogénèse des tubules-T dans le muscle squelettique et dans la physiopathologie des cavéolinopathies
In skeletal muscle, invaginations of the sarcolemma called caveolae and their main component Cav-3 are thought to be involved in the formation of transverse tubules. T-tubules are muscle structures that allow the action potential to be propagated into the muscle fibre. However, the mechanism linking them together remains unknown. The importance of caveolae and Cav-3 is accentuated by the existence of defects in the organisation and function of caveolae in caveolinopathies, autosomal dominant neuromuscular diseases due to mutations in the CAV-3 gene, the pathophysiological mechanisms of which are still not understood. The objective of my project was to understand the role of caveolae in the early formation of T-tubules. A correlative microscopy technique combining super-resolution fluorescence and electron microscopy on metal replicas was used to examine in detail the molecular components of caveolae and T-tubules in extensively differentiated myotubes. I showed the organisation of caveolae on Bin1 platforms forming a novel ring structure that appears to optimise membrane tubulation in the initiation of T-tubule formation. These rings and Bin1-mediated membrane tubulation are impaired in Cav-3 expression defects and in myotubes from caveolinopathic patients. My work suggests that caveolae rings are the site of T-tubule initiation and provides the basis for characterising T-tubule biogenesis in skeletal muscle and in the pathophysiology of caveolinopathies
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Wagner, Eva [Verfasser], Stephan E. [Akademischer Betreuer] Lehnart, Michael [Akademischer Betreuer] Hoppert, and Stefan [Akademischer Betreuer] Jakobs. "Cardiac T-Tubule Membranes - Nanostructure and Remodeling Mechanisms in Disease / Eva Wagner. Gutachter: Michael Hoppert ; Stefan Jakobs. Betreuer: Stephan E. Lehnart." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://d-nb.info/1044768428/34.

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Afrin, Sadia. "Defining a 3-dimensional (3D) in vitro model to study immune cell and renal cell interactions." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/84754/1/Sadia_Afrin_Thesis.pdf.

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This study aimed to develop a 3-Dimensional (D) hydrogel system for the co-culture of autologous human renal and immune cells. Previous studies have shown that human renal epithelial cells are able to modulate autologous immune cell responses. However, these studies were undertaken in a standard 2D culture system. The 3D model was developed to re-capitulate these observations within a more physiological relevant in vivo like environment.
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Metzger, Sabrina Kinzie. "Modeling of excitation in skeletal muscle." Wright State University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1620983611677044.

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Payne, J. G. "Residual stresses in welded tubular T-joints." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384523.

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Neira, Dorivalda Santos Medeiros. "Fibras de sisal (Agave sisalana) como isolante t?rmico de tubula??es." Universidade Federal do Rio Grande do Norte, 2005. http://repositorio.ufrn.br:8080/jspui/handle/123456789/15545.

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Made available in DSpace on 2014-12-17T14:57:45Z (GMT). No. of bitstreams: 1 DorivaldaSMN.pdf: 3293308 bytes, checksum: e37080f4f72e81ac421fcaf0fec21fa8 (MD5) Previous issue date: 2005-12-16
Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico
In the last decades there was a significant increasing of the numbers of researchers that joint efforts to find alternatives to improve the development of low environmental impact technology. Materials based on renewable resources have enormous potentials of applications and are seen as alternatives for the sustainable development. Within other parameters, the sustainability depends on the energetic efficiency, which depends on the thermal insulation. Alternative materials, including vegetal fibers, can be applied to thermal insulation, where its first goal is to minimize the loss of energy. In the present research, it was experimentally analyzed the thermal behavior of fiber blankets of sisal (Agave sisalana) with and without surface treatment with oxide hidroxide (NaOH). Blankets with two densities (1100/1200 and 1300/1400 g/m2) were submitted to three rates of heat transfer (22.5 W, 40 W and 62.5 W). The analysis of the results allowed comparing the blankets treated and untreated in each situation. Others experiments were carried out to obtain the thermal conductivity (k), heat capacity (C) and the thermal diffusivity (α) of the blankets. Thermo gravimetric analyses were made to the verification of the thermal stability. Based on the results it was possible to relate qualitatively the effect of the heat transfer through the sisal blankets subjected to three heat transfer rates, corresponding to three temperature values (77 ?C, 112 ?C e 155 ?C). To the first and second values of temperature it was verified a considerable reduction on the rate of heat transfer; nevertheless, to the third value of temperature, the surface of the blankets (treated and untreated) in contact with the heated surface of the tube were carbonized. It was also verified, through the analyses of the results of the measurements of k, C e α, that the blankets treated and untreated have values near to the conventional isolating materials, as glass wool and rock wool. It could be concluded that is technically possible the use of sisal blankets as constitutive material of thermal isolation systems in applications where the temperature do not reach values greater than 112 ?C
Nas ?ltimas d?cadas, t?m sido grandes os esfor?os dos pesquisadores na busca por alternativas sustent?veis e conhecimentos sobre como se poder? continuar promovendo o desenvolvimento sem que isso ocorra de forma agressiva ao ambiente. Materiais oriundos de fontes renov?veis possuem grande potencial de aplicabilidade e s?o vistos como alternativas para um desenvolvimento sustent?vel. Dentre outros par?metros, a sustentabilidade depende da efici?ncia energ?tica e essa, por sua vez, depende de isolantes t?rmicos. Materiais alternativos, entre eles as fibras vegetais, podem ser aplicadas para fins de isolamento t?rmico, cujo principal objetivo ? minimizar as perdas de energia. Na presente pesquisa, analisou-se experimentalmente a aplicabilidade de mantas de fibras de sisal (Agave sisalana), in natura e com tratamento superficial com hidr?xido de s?dio (NaOH), ? isola??o t?rmica. Foram utilizadas mantas de duas gramaturas (1100/1200 e 1300/1400 g/m2) submetidas a tr?s taxas de transfer?ncia de calor (22,5 W, 40 W e 62,5 W). A an?lise dos resultados obtidos permitiu comparar a capacidade de isola??o das mantas tratada e in natura em cada situa??o. Ensaios foram realizados para determina??o da condutividade t?rmica (k), capacidade calor?fica (C) e a difusividade t?rmica (α) das mantas; a estabilidade t?rmica foi verificada por meio de an?lise termogravim?trica (TGA). Com base nos resultados, foi poss?vel relacionar qualitativamente o efeito da transfer?ncia de calor atrav?s das mantas de sisal submetidas a tr?s condi??es de aquecimento, correspondentes a tr?s valores de temperatura (77 ?C, 112 ?C e 155 ?C). Nas duas condi??es iniciais, verificou-se que as mantas de sisal proporcionaram uma significativa redu??o da taxa de transfer?ncia de calor. Na terceira condi??o (155 ?C), contudo, as superf?cies das mantas (tratadas e in natura) em contato com a superf?cie aquecida do tubo ficaram carbonizadas. Por meio das an?lises dos resultados das medi??es de k, C e α, constatou-se que as mantas tratadas e in natura apresentaram valores bem pr?ximos aos de materiais isolantes comerciais (l? de vidro e l? de rocha). P?de-se concluir que mantas de sisal podem ser empregadas como material constituinte de sistemas de isola??o t?rmica para aplica??es em que a temperatura n?o ultrapasse 112 ?C
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Li, Qince. "Mathematical modelling of intracellular Ca2+ alternans in atrial and ventricular myocytes." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/mathematical-modelling-of-intracellular-ca2-alternans-in-atrial-and-ventricular-myocytes(54ff4d2a-f820-43b6-a572-4706850f28ec).html.

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During excitation-contraction coupling, Ca2+ transient induced by the depolarization of membrane potential is the trigger of mechanical contraction in cardiac myocytes, which is responsible for the pumping function of the heart. However, mechanisms underlying intracellular Ca2+ regulation and the coupling between Ca2+ transient and membrane potential are not completely understood. Abnormalities in intracellular Ca2+ regulation have been observed during heart failure and cardiac arrhythmias, such as intracellular Ca2+ alternans and T-tubule disorganization. In this project, intracellular Ca2+ dynamics in different types of cardiac myocytes were investigated by using computer modelling. For atrial myocytes, a biophysically detailed computer model was developed to describe the observations of Ca2+ alternans and Ca2+ wave propagation in cardiac myocytes lacking T-tubules. The model was validated by its ability to reproduce experimental observed Ca2+ wave propagation under normal condition and the influences on spatial Ca2+ distribution by modifying various aspects of Ca2+ cycling, such as Ca2+ influx, SR Ca2+ uptake and SR Ca2+ release in cardiac myocytes lacking T-tubules. Mechanisms underlying the genesis of Ca2+ alternans in this type of cell were investigated by the model. Furthermore, a spontaneous second Ca2+ release was observed in response to a single voltage stimulus pulse with enhanced Ca2+ influx as well as SR Ca2+ overload. For the ventricular myocytes, an existing canine model was used to study the genesis of APD and intracellular Ca2+ alternans under various conditions. The genesis of Ca2+ alternans was investigated by analyzing the relationship between systolic Ca2+ concentration and SR Ca2+ content. On the other side, the roles of SR Ca2+ regulation and action potential restitution in the genesis of intracellular Ca2+ and APD alternans were also examined under various conditions. In addition, it was shown that spatially discordant Ca2+ alternans was generated when the Ca2+-dependent inactivation of ICa,L was strong. It tended to be concordant for weak Ca2+-dependent inactivation of ICa,L. For the sinoatrial node cells, a mathematical model was developed to simulate stochastic opening of unitary L-type Ca2+ channel and single RyR channel, thereby reproducing experimental observed local Ca2+ release during diastolic depolarization phase of the action potential. Simulation results of ionic channel block and modifications of SR Ca2+ regulation suggested a limited role of intracellular Ca2+ in the automaticity of central SA node cells.
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Books on the topic "Tubule-T"

1

Crawford, D. G. Fatigue crack growth in medium scale tubular T-joints under variable amplitude loading. EastKilbride: National Engineering Laboratory, 1990.

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2

Kanitkar, Ravindra V. Numerical investigation of typical rectangular welded tubular T and DT-joints. 1993.

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The Static Strength of Uniplanar and Multiplanar Tubular T- And X-Joints. Delft Univ Pr, 1995.

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4

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

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.

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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.
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Book chapters on the topic "Tubule-T"

1

Sipido, Karin R., Károly Acsai, Gudrun Antoons, Virginie Bito, and Niall Macquaide. "T-Tubule Remodelling and Ryanodine Receptor Organization Modulate Sodium-Calcium Exchange." In Advances in Experimental Medicine and Biology, 375–83. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_32.

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Arampatzis, Adamantios, Lida Mademli, Thomas Reilly, Mike I. Lambert, Laurent Bosquet, Jean-Paul Richalet, Thierry Busso, et al. "T-Tubules." In Encyclopedia of Exercise Medicine in Health and Disease, 883. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3149.

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Öz, A. M., S. M. J. Dunn, and G. B. Frank. "45Ca++ Efflux Studies in Rabbit T-Tubule Membrane Preparations in the Range of Late After Potentials During Tetanic Contractions." In Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle, 419–21. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3362-7_62.

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Dohm, G. Lynis, and Ronald W. Dudek. "Role of Transverse Tubules (T-Tubules) in Muscle Glucose Transport." In Advances in Experimental Medicine and Biology, 27–34. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-1928-1_3.

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Zheng, Jianmin, and Yimin Wang. "Periodic T-Splines and Tubular Surface Fitting." In Curves and Surfaces, 731–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-27413-8_48.

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Venosa, R. A. "Sodium Pump in T-Tubules of Frog Muscle Fibers." In Transduction in Biological Systems, 275–86. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5736-0_19.

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Rog-Zielinska, Eva A. "Structure of Transverse (T)-Tubules in Health and Disease." In Heart Rate and Rhythm, 347–57. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-33588-4_16.

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8

Maddox, S. J. "Fatigue crack growth in tubular T-joints under in-plane bending." In Tubular Structures VII, 285–92. London: Routledge, 2022. http://dx.doi.org/10.1201/9780203735008-43.

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Maddox, S. J. "Fatigue crack growth in tubular T-joints under in-plane bending." In Tubular Structures VII, 285–92. London: Routledge, 2022. http://dx.doi.org/10.1201/9780203735008-43.

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10

Frank, George B., and Murat Öz. "The Functional Role of T-Tubular Calcium Channels in Skeletal Muscle Contractions." In Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle, 123–36. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3362-7_9.

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Conference papers on the topic "Tubule-T"

1

Prins, K., L. Rose, L. Tian, D. Wu, T. Thenappan, and S. L. Archer. "Interleukin-6 as a Potential Modulator of Right Ventricular Function Via the Microtubule-Junctophilin-2-T-Tubule Pathway." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2797.

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Dong, Pingsha, and Jeong K. Hong. "Fatigue of Tubular Joints: Hot Spot Stress Method Revisited." In ASME 2008 27th International Conference on Offshore Mechanics and Arctic Engineering. ASMEDC, 2008. http://dx.doi.org/10.1115/omae2008-57914.

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A series of well-known tubular joints tested in UKSORP II have been re-evaluated using the mesh-insensitive structural stress method as a part of the on-going Battelle Structural Stress JIP efforts. In this report, the structural stress based analysis procedure is first presented for applications in tubular joints varying from simple T joints, double T Joints, YT joints with overlap and K joints with various internal stiffening configurations. The structural stress based SCFs are then compared with those obtained using traditional surface extrapolation based hot spot stress methods. Their abilities in effectively correlating the fatigue data collected from these tubular joints are demonstrated. These tests are also compared with the T curve typically used for fatigue design of tubular joints as well as the structural stress based master S-N curve adopted by ASME Section VIII Div 2. Finally, some of the implications on fracture mechanics based remaining life assessment for tubular joints are discussed in light of the results obtained in this investigation.
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Manabe, Ken-ichi, Kenta Itai, and Kazuo Tada. "Fabrication of micro T-shaped tubular components by hydroforming process." In PROCEEDINGS OF THE INTERNATIONAL CONFERENCE OF GLOBAL NETWORK FOR INNOVATIVE TECHNOLOGY AND AWAM INTERNATIONAL CONFERENCE IN CIVIL ENGINEERING (IGNITE-AICCE’17): Sustainable Technology And Practice For Infrastructure and Community Resilience. Author(s), 2017. http://dx.doi.org/10.1063/1.5008062.

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Deng, Peng, Benbing Li, Huiling Wang, and Qibiao Zhang. "Experimental Research on Hysteretic Behaviors of Square Tubular T-joint." In 2015 International Conference on Materials, Environmental and Biological Engineering. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/mebe-15.2015.43.

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Baczkiewicz, Jolanta, Mikko Malaska, Sami Pajunen, Mika Alanen, and Markku Heinisuo. "Experimental Study on Tubular Steel t-joints Under Fire Conditions." In Proceedings of the 17th International Symposium on Tubular Structures(ISTS17). Singapore: Research Publishing Services, 2019. http://dx.doi.org/10.3850/978-981-11-0745-0_016-cd.

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Haagensen, P. J., and B. Skallerud. "Fatigue Assessment and Testing of a Repaired Tubular T-Joint." In ASME 2004 23rd International Conference on Offshore Mechanics and Arctic Engineering. ASMEDC, 2004. http://dx.doi.org/10.1115/omae2004-51262.

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Stress concentration factors (SCF’s) for a T-joint were calculated by parametric equations, finite element analysis, weight functions, and by experimental stress analysis. Fatigue life predictions were made on the basis of computed SCF’s. Fatigue tests were performed to determine crack development and fatigue life. Following crack growth through the thickness, the crack was ground out and the joint repaired by welding and improved by peening. Further testing at a 35% higher load showed that the original fatigue life was restored by the repair.
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7

Makino, Y., Y. Kurobane, S. Takizawa, and N. Yamamoto. "Behavior Of Tubular T- and K-Joints Under Combined Loads." In Offshore Technology Conference. Offshore Technology Conference, 1986. http://dx.doi.org/10.4043/5133-ms.

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8

Lie, S. T., S. P. Chiew, and S. Sun. "Experimental investigation of T-tubular joint subjected to complex loading conditions." In Second International Conference on Experimental Mechanics, edited by Fook S. Chau and Chenggen Quan. SPIE, 2001. http://dx.doi.org/10.1117/12.429601.

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9

Liu, Jian-ping. "Study on the ultimate strength of internal stiffened square tubular T-joints." In 2011 International Conference on Electric Technology and Civil Engineering (ICETCE). IEEE, 2011. http://dx.doi.org/10.1109/icetce.2011.5776320.

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10

Sun, Peng, Yuanqing Wang, and Yongjiu Shi. "Non-Linear Analysis for Ultimate Loading Capacity of Cast Tubular T-Joints." In ASME 2005 24th International Conference on Offshore Mechanics and Arctic Engineering. ASMEDC, 2005. http://dx.doi.org/10.1115/omae2005-67309.

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In this paper, we performed a lot of parametric analysis of cast T-joints. The geometry model was established using Solidworks. Non-linear analysis was carried out using the commercial finite element programme Ansys. Parametric equations of ultimate loading capacity derived from the results of finite element analysis are presented for the usual range of basic shapes of T-joints under axial loading, in-plane and out-of-plane bending. The sensitivity of the ultimate loading capacity in cast tubular joints to variation in the geometric parameters has been assessed. Besides the parameters which governing the stresses in welded joints, an additional parameter ρ that is defined by C. D. Edwards has been introduced to describe the size of fillet. In this paper, the sensitivity of ultimate loading capacity of cast tubular joints to the parameter ρ is presented.
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Reports on the topic "Tubule-T"

1

Musa, Idris A., and Fidelis R. Mashiri. PARAMETRIC STUDY ON CONCRETE-FILLED STEEL TUBULAR T-JOINTS UNDER IN-PLANE BENDING. The Hong Kong Institute of Steel Construction, December 2018. http://dx.doi.org/10.18057/icass2018.p.113.

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2

Yiran, Wu, Meng Lingye, and Shi Yongjiu. INVESTIGATIONS OF JOINTS STRENGTH PERFORMANCE WITH T-SECTION CONCRETE FILLED STEEL TUBULAR COLUMNS AND I-SECTION STEEL BEAMS. The Hong Kong Institute of Steel Construction, December 2018. http://dx.doi.org/10.18057/icass2018.p.027.

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3

ANALYSIS OF THE DYNAMIC MECHANISM OF SQUARE TUBULAR T-JOINTS WITH CHORD FLANGES SUBJECTED TO IMPACT LOADING. The Hong Kong Institute of Steel Construction, March 2024. http://dx.doi.org/10.18057/ijasc.2024.20.1.3.

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This study examines the dynamic mechanical properties of square tubular T-joints with impact loads acting on the chord surface in the joint area. The study first verified the failure modes and behaviors of the specimens under a brace axial force and impact, respectively, where the simulation results demonstrated good agreement with the experimental results. A total of 138 square hollow section tubular T-joint finite element models were divided into T1, T2, and T3 groups based on different tube diameter ratios. The failure modes, displacement-time history curves, and impact force-time history curves were obtained. The results revealed that the joint deformation modes were primarily characterized by significant local indentation at the impact site and junction of the chord and brace, as well as a certain degree of deformation at both ends of the chord. Within a certain range, the preloaded axial force could mitigate the development of plastic deformation, whereas an increased ratio of the drop hammer length to chord diameter exacerbated it. Finally, theoretical analysis was simplified by defining the plastic element set, and the energy dissipation coefficient ψ was proposed to evaluate the impact resistance of square tubular T-joints by analyzing the specific energy changes in the intersecting region (El) and at the ends of the chord (Ee).
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4

EXPERIMENTAL INVESTIGATION ON COLD-FORMED HIGH STRENGTH STEEL TUBULAR T-JOINTS. The Hong Kong Institute of Steel Construction, December 2018. http://dx.doi.org/10.18057/icass2018.p.007.

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5

LOW-TEMPERATURE COMPRESSION BEHAVIOUR OF CIRCULAR STUB STAINLESS-STEEL TUBULAR COLUMNS. The Hong Kong Institute of Steel Construction, September 2022. http://dx.doi.org/10.18057/ijasc.2022.18.3.4.

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This paper firstly studies mechanical properties of stainless steel (SS) S30408 at the low temperature (T) range of -80~20℃. Further compression tests are carried out on 20 SS stub tubular columns (SSSTCs) at low temperatures of -80, -60, -30, and 20℃ to investigate their low-temperature compression behaviour. Including the testing low temperatures, the wall thickness of SS tube (t) is the other investigated parameters. Test results show that decreasing the T from 20 to -80℃ improves the yield and ultimate strength of stainless steel by 29% and 80%, respectively, but reduces its ductility by about 25%. Under low-temperature compression, elephant foot local buckling occurs to most of SSSTCs and inelastic inward and outward local buckling occurred to specimens with 6 mm-thick SS tube. Test results also show that the decreasing T value increases the strength and stiffness of SSSTCs, but compromises their ductility; the wall thickness of SSSTCs significantly improves their strength, stiffness, and ductility. This paper also develops 3D finite element model (FEM) to estimate the low-temperature compression behaviour of SSSTCs, which considers nonlinearities of material and geometry, geometric imperfections, and influences of low temperatures. The validations show it predicts reasonably well the low-temperature compression behaviours of SSSTCs.
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