Relevant bibliographies by topics / Engineered Heart Muscle Tissues

Academic literature on the topic 'Engineered Heart Muscle Tissues'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Engineered Heart Muscle Tissues"

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Sheehy, Sean P., Anna Grosberg, Pu Qin, David J. Behm, John P. Ferrier, Mackenzie A. Eagleson, Alexander P. Nesmith, et al. "Toward improved myocardial maturity in an organ-on-chip platform with immature cardiac myocytes." Experimental Biology and Medicine 242, no. 17 (March 26, 2017): 1643–56. http://dx.doi.org/10.1177/1535370217701006.

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In vitro studies of cardiac physiology and drug response have traditionally been performed on individual isolated cardiomyocytes or isotropic monolayers of cells that may not mimic desired physiological traits of the laminar adult myocardium. Recent studies have reported a number of advances to Heart-on-a-Chip platforms for the fabrication of more sophisticated engineered myocardium, but cardiomyocyte immaturity remains a challenge. In the anisotropic musculature of the heart, interactions between cardiac myocytes, the extracellular matrix (ECM), and neighboring cells give rise to changes in cell shape and tissue architecture that have been implicated in both development and disease. We hypothesized that engineered myocardium fabricated from cardiac myocytes cultured in vitro could mimic the physiological characteristics and gene expression profile of adult heart muscle. To test this hypothesis, we fabricated engineered myocardium comprised of neonatal rat ventricular myocytes with laminar architectures reminiscent of that observed in the mature heart and compared their sarcomere organization, contractile performance characteristics, and cardiac gene expression profile to that of isolated adult rat ventricular muscle strips. We found that anisotropic engineered myocardium demonstrated a similar degree of global sarcomere alignment, contractile stress output, and inotropic concentration–response to the β-adrenergic agonist isoproterenol. Moreover, the anisotropic engineered myocardium exhibited comparable myofibril related gene expression to muscle strips isolated from adult rat ventricular tissue. These results suggest that tissue architecture serves an important developmental cue for building in vitro model systems of the myocardium that could potentially recapitulate the physiological characteristics of the adult heart. Impact statement With the recent focus on developing in vitro Organ-on-Chip platforms that recapitulate tissue and organ-level physiology using immature cells derived from stem cell sources, there is a strong need to assess the ability of these engineered tissues to adopt a mature phenotype. In the present study, we compared and contrasted engineered tissues fabricated from neonatal rat ventricular myocytes in a Heart-on-a-Chip platform to ventricular muscle strips isolated from adult rats. The results of this study support the notion that engineered tissues fabricated from immature cells have the potential to mimic mature tissues in an Organ-on-Chip platform.
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He, Feng, Hailan Yao, Jianmin Wang, Zonghui Xiao, Le Xin, Zhuo Liu, Xiaolin Ma, Juan Sun, Qi Jin, and Zhewei Liu. "Coxsackievirus B3 Engineered To Contain MicroRNA Targets for Muscle-Specific MicroRNAs Displays Attenuated Cardiotropic Virulence in Mice." Journal of Virology 89, no. 2 (October 22, 2014): 908–16. http://dx.doi.org/10.1128/jvi.02933-14.

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ABSTRACTCoxsackievirus B3 (CVB3) is trophic for cardiac tissue and is a major causative agent for viral myocarditis, where local viral replication in the heart may lead to heart failure or even death. Recent studies show that inserting microRNA target sequences into the genomes of certain viruses can eradicate these viruses within local host tissues that specifically express the cognate microRNA. Here, we demonstrated bothin vitroandin vivothat incorporating target sequences for miRNA-133 and -206 into the 5′ untranslated region of the CVB3 genome ameliorated CVB3 virulence in skeletal muscle and myocardial cells that specifically expressed the cognate cellular microRNAs. Compared to wild-type CVB3, viral replication of the engineered CVB3 was attenuated in human TE671 (rhabdomyosarcoma) and L6 (skeletal muscle) cell linesin vitrothat expressed high levels of miRNA-206. In thein vivomurine CVB3-infection model, viral replication of the engineered CVB3 was attenuated specifically in the heart that expressed high levels of both miRNAs, but not in certain tissues, which allowed the host to retain the ability to induce a strong and protective humoral immune response against CVB3. The results of this study suggest that a microRNA-targeting strategy to control CVB3 tissue tropism and pathogenesis may be useful for viral attenuation and vaccine development.IMPORTANCECoxsackievirus B3 (CVB3) is a major causative agent for viral myocarditis, and viral replication in the heart may lead to heart failure or even death. Limiting CVB3 replication within the heart may be a promising strategy to decrease CVB3 pathogenicity. miRNAs are ∼21-nucleotide-long, tissue-specific endogenous small RNA molecules that posttranscriptionally regulate gene expression by imperfectly binding to the 3′ untranslated region (UTR), the 5′ UTR, or the coding region within a gene. In our study, muscle-specific miRNA targets (miRT) were incorporated into the CVB3 genome. Replication of the engineered viruses was restricted in the important heart tissue of infected mice, which reduced cardiac pathology and increased mouse survival. Meanwhile, replication ability was retained in other tissues, thus inducing a strong humoral immune response and providing long-term protection against CVB3 rechallenge. This study suggests that a microRNA-targeting strategy can potentially control CVB3 tissue tropism and pathogenesis and may be useful for viral attenuation and vaccine development.
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Schmitt, Phillip R., Kiera D. Dwyer, Alicia J. Minor, and Kareen L. K. Coulombe. "Wet-Spun Polycaprolactone Scaffolds Provide Customizable Anisotropic Viscoelastic Mechanics for Engineered Cardiac Tissues." Polymers 14, no. 21 (October 28, 2022): 4571. http://dx.doi.org/10.3390/polym14214571.

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Myocardial infarction is a leading cause of death worldwide and has severe consequences including irreversible damage to the myocardium, which can lead to heart failure. Cardiac tissue engineering aims to re-engineer the infarcted myocardium using tissues made from human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to regenerate heart muscle and restore contractile function via an implantable epicardial patch. The current limitations of this technology include both biomanufacturing challenges in maintaining tissue integrity during implantation and biological challenges in inducing cell alignment, maturation, and coordinated electromechanical function, which, when overcome, may be able to prevent adverse cardiac remodeling through mechanical support in the injured heart to facilitate regeneration. Polymer scaffolds serve to mechanically reinforce both engineered and host tissues. Here, we introduce a novel biodegradable, customizable scaffold composed of wet-spun polycaprolactone (PCL) microfibers to strengthen engineered tissues and provide an anisotropic mechanical environment to promote engineered tissue formation. We developed a wet-spinning process to produce consistent fibers which are then collected on an automated mandrel that precisely controls the angle of intersection of fibers and their spacing to generate mechanically anisotropic scaffolds. Through optimization of the wet-spinning process, we tuned the fiber diameter to 339 ± 31 µm and 105 ± 9 µm and achieved a high degree of fidelity in the fiber structure within the scaffold (fiber angle within 1.8° of prediction). Through degradation and mechanical testing, we demonstrate the ability to maintain scaffold mechanical integrity as well as tune the mechanical environment of the scaffold through structure (Young’s modulus of 120.8 ± 1.90 MPa for 0° scaffolds, 60.34 ± 11.41 MPa for 30° scaffolds, 73.59 ± 3.167 MPa for 60° scaffolds, and 49.31 ± 6.90 MPa for 90° scaffolds), while observing decreased hysteresis in angled vs. parallel scaffolds. Further, we embedded the fibrous PCL scaffolds in a collagen hydrogel mixed with hiPSC-CMs to form engineered cardiac tissue with high cell survival, tissue compaction, and active contractility of the hiPSC-CMs. Through this work, we develop and optimize a versatile biomanufacturing process to generate customizable PCL fibrous scaffolds which can be readily utilized to guide engineered tissue formation and function.
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Naito, H. "Optimizing Engineered Heart Tissue for Therapeutic Applications as Surrogate Heart Muscle." Circulation 114, no. 1_suppl (July 4, 2006): I—72—I—78. http://dx.doi.org/10.1161/circulationaha.105.001560.

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Porzionato, Andrea, Elena Stocco, Silvia Barbon, Francesca Grandi, Veronica Macchi, and Raffaele De Caro. "Tissue-Engineered Grafts from Human Decellularized Extracellular Matrices: A Systematic Review and Future Perspectives." International Journal of Molecular Sciences 19, no. 12 (December 18, 2018): 4117. http://dx.doi.org/10.3390/ijms19124117.

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Tissue engineering and regenerative medicine involve many different artificial and biologic materials, frequently integrated in composite scaffolds, which can be repopulated with various cell types. One of the most promising scaffolds is decellularized allogeneic extracellular matrix (ECM) then recellularized by autologous or stem cells, in order to develop fully personalized clinical approaches. Decellularization protocols have to efficiently remove immunogenic cellular materials, maintaining the nonimmunogenic ECM, which is endowed with specific inductive/differentiating actions due to its architecture and bioactive factors. In the present paper, we review the available literature about the development of grafts from decellularized human tissues/organs. Human tissues may be obtained not only from surgery but also from cadavers, suggesting possible development of Human Tissue BioBanks from body donation programs. Many human tissues/organs have been decellularized for tissue engineering purposes, such as cartilage, bone, skeletal muscle, tendons, adipose tissue, heart, vessels, lung, dental pulp, intestine, liver, pancreas, kidney, gonads, uterus, childbirth products, cornea, and peripheral nerves. In vitro recellularizations have been reported with various cell types and procedures (seeding, injection, and perfusion). Conversely, studies about in vivo behaviour are poorly represented. Actually, the future challenge will be the development of human grafts to be implanted fully restored in all their structural/functional aspects.
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Skopenkova, Victoria V., Tatiana V. Egorova, and Maryana V. Bardina. "Muscle-Specific Promoters for Gene Therapy." Acta Naturae 13, no. 1 (March 15, 2021): 47–58. http://dx.doi.org/10.32607/actanaturae.11063.

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Many genetic diseases that are responsible for muscular disorders have been described to date. Gene replacement therapy is a state-of-the-art strategy used to treat such diseases. In this approach, the functional copy of a gene is delivered to the affected tissues using viral vectors. There is an urgent need for the design of short, regulatory sequences that would drive a high and robust expression of a therapeutic transgene in skeletal muscles, the diaphragm, and the heart, while exhibiting limited activity in non-target tissues. This review focuses on the development and improvement of muscle-specific promoters based on skeletal muscle -actin, muscle creatine kinase, and desmin genes, as well as other genes expressed in muscles. The current approaches used to engineer synthetic muscle-specific promoters are described. Other elements of the viral vectors that contribute to tissue-specific expression are also discussed. A special feature of this review is the presence of up-to-date information on the clinical and preclinical trials of gene therapy drug candidates that utilize muscle-specific promoters.
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Birla, Ravi K., Gregory H. Borschel, and Robert G. Dennis. "In Vivo Conditioning of Tissue-engineered Heart Muscle Improves Contractile Performance." Artificial Organs 29, no. 11 (November 2005): 866–75. http://dx.doi.org/10.1111/j.1525-1594.2005.00148.x.

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Santos, Gabriela Leão, Svenja Hartmann, Wolfram-Hubertus Zimmermann, Anne Ridley, and Susanne Lutz. "Inhibition of Rho-associated kinases suppresses cardiac myofibroblast function in engineered connective and heart muscle tissues." Journal of Molecular and Cellular Cardiology 134 (September 2019): 13–28. http://dx.doi.org/10.1016/j.yjmcc.2019.06.015.

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Buckner, Frederick S., Aaron J. Wilson, and Wesley C. Van Voorhis. "Detection of Live Trypanosoma cruzi in Tissues of Infected Mice by Using Histochemical Stain for β-Galactosidase." Infection and Immunity 67, no. 1 (January 1, 1999): 403–9. http://dx.doi.org/10.1128/iai.67.1.403-409.1999.

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ABSTRACT The pathogenesis of tissue damage in chronic Trypanosoma cruzi infection has been a subject of long-standing debate. Conventional staining methods reveal a paucity of parasites in tissues from chronically infected individuals, which has led to the theory that the pathologic findings may be primarily autoimmune in origin. Immunostaining for T. cruzi antigens or in situ PCR methods show evidence for parasite components in chronic tissues; however, these methods do not address whether the stained material represents parasite debris or live organisms. An improved method for detecting intact T. cruzi in tissues was developed by making a genetically engineered strain that expresses Escherichia coli β-galactosidase. The expression of this enzyme allows the detection of T. cruzi in tissues by using the histochemical stain 5-bromo-4-chloro-3-indolyl-β-d-galactopyranoside (X-Gal). The technique was used to monitor tissue parasitism and its relation to pathologic findings in the mouse model of Chagas’ disease. Parasites were easily visible as bright blue structures in skeletal muscle, heart, bladder, peripheral nerve, liver, spleen, adrenal gland, brain, and adipose tissue in acutely infected mice. The number of viable parasites diminished >100-fold when tissues from 3-week-infected mice were compared with those from 10-month-infected mice. However, even at the lower level, parasites were clearly recognizable in sections of skeletal muscle and bladder at the 10-month time point. Inflammation remained robust in skeletal muscle, bladder, and sciatic nerve despite the near disappearance of parasites, suggesting three possibilities: exuberant host reactions to the few remaining parasites, autoimmune inflammation, or reactions to retained parasite antigens in the tissues.
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Bremner, Samantha B., Christian J. Mandrycky, Andrea Leonard, Ruby M. Padgett, Alan R. Levinson, Ethan S. Rehn, J. Manuel Pioner, Nathan J. Sniadecki, and David L. Mack. "Full-length dystrophin deficiency leads to contractile and calcium transient defects in human engineered heart tissues." Journal of Tissue Engineering 13 (January 2022): 204173142211196. http://dx.doi.org/10.1177/20417314221119628.

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Cardiomyopathy is currently the leading cause of death for patients with Duchenne muscular dystrophy (DMD), a severe neuromuscular disorder affecting young boys. Animal models have provided insight into the mechanisms by which dystrophin protein deficiency causes cardiomyopathy, but there remains a need to develop human models of DMD to validate pathogenic mechanisms and identify therapeutic targets. Here, we have developed human engineered heart tissues (EHTs) from CRISPR-edited, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) expressing a truncated dystrophin protein lacking part of the actin-binding domain. The 3D EHT platform enables direct measurement of contractile force, simultaneous monitoring of Ca2+ transients, and assessment of myofibril structure. Dystrophin-mutant EHTs produced less contractile force as well as delayed kinetics of force generation and relaxation, as compared to isogenic controls. Contractile dysfunction was accompanied by reduced sarcomere length, increased resting cytosolic Ca2+ levels, delayed Ca2+ release and reuptake, and increased beat rate irregularity. Transcriptomic analysis revealed clear differences between dystrophin-deficient and control EHTs, including downregulation of genes related to Ca2+ homeostasis and extracellular matrix organization, and upregulation of genes related to regulation of membrane potential, cardiac muscle development, and heart contraction. These findings indicate that the EHT platform provides the cues necessary to expose the clinically-relevant, functional phenotype of force production as well as mechanistic insights into the role of Ca2+ handling and transcriptomic dysregulation in dystrophic cardiac function, ultimately providing a powerful platform for further studies in disease modeling and drug discovery.
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Dissertations / Theses on the topic "Engineered Heart Muscle Tissues"

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Fernández, Garibay Xiomara Gislen. "Engineered functional skeletal muscle tissues for in vitro studies." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673232.

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The skeletal muscle is the largest tissue of the human body. Its main function is to generate contractile forces, essential for locomotion, thermogenesis, and metabolism. Fundamental research on skeletal muscle in health and disease, and preclinical research for new therapies, are currently based on 2D in vitro cell cultures and in vivo animal models. However, these strategies have important shortcomings. For instance, conventional cell culture models cannot emulate the complex 3D architecture of native skeletal muscle, and the species-specific differences in animal models limit their relevance to humans. In contrast, engineered skeletal muscle tissues are emerging as in vitro 3D cell culture models that complement existing 2D strategies. These engineered tissues can offer an improved microenvironment resembling native muscle tissue, comprised of bundles of aligned, multinucleated fibers. Therefore, the main objective of this thesis was to develop 3D skeletal muscle tissues for in vitro studies of muscle metabolism and disease modeling. Skeletal muscle precursor cells were encapsulated in microfabricated hydrogel scaffolds, introducing the appropriate topographical and microenvironmental cues to guide muscle fiber formation. First, photocrosslinkable gelatin methacryloyl (GelMA)-based composite hydrogels were synthesized and evaluated as cell-laden bioinks for 3D bioprinting of murine skeletal muscle tissue. The fabrication conditions were optimized to ensure the biocompatibility of the process and promote in vitro myogenesis. Our results demonstrated that the composite hydrogels have a higher resistance to degradation than GelMA hydrogels. Thus, the bioprinted scaffolds maintained their 3D structure over a prolonged culture period. Furthermore, the shear stress during extrusion bioprinting combined with the appropriate scaffold geometry resulted in highly aligned myoblasts that correctly differentiated into multinucleated myotubes. Considering these results, GelMA-carboxymethylcellulose methacrylate (CMCMA) hydrogels were then used to generate skeletal muscle microtissues in long-lasting cell cultures. Photomold patterning of cell-laden GelMA-CMCMA filaments led to the formation of highly aligned 3D myotubes expressing sarcomeric proteins. Moreover, the presented protocols were highly biocompatible and reproducible. Murine skeletal muscle microtissues were fabricated in a microfluidic platform integrated with an electrical stimulation system and biosensors for monitoring muscle metabolism in situ. Here, we measured the contraction-induced release of muscle-secreted cytokines upon electrical or biological stimulation. The obtained results confirmed the endocrine function of the bioengineered tissues, obtaining in vivo-like responses upon exercise or endotoxin-induced inflammation. Then, the photomold patterning protocol was optimized for human cells to develop the first in vitro 3D model of myotonic dystrophy type 1 (DM1) human skeletal muscle. DM1 is the most prevalent hereditary myopathy in adults, and there is no effective treatment to date. We proved that 3D micropatterning enhances DM1 myotube formation compared to 2D cultures. Furthermore, we detected the reduced thickness of 3D DM1 myotubes compared to healthy controls, which was proposed as a new in vitro structural phenotype. Thus, as a proof-of-concept, we demonstrated that treatment with an antisense oligonucleotide, antagomiR-23b, could rescue both molecular and structural phenotypes in these bioengineered DM1 muscle tissues. Finally, animal-derived components were eliminated to develop in vitro functional tissues in xeno-free cell culture as a next step towards improving bioengineered human skeletal muscle tissues. Cell-laden nanocomposite hydrogels consisting of human platelet lysate and functionalized cellulose nanocrystals (HUgel) were fabricated in hydrogel casting platforms that implemented uniaxial tension during matrix remodeling. We modulated the content of cellulose nanocrystals to tune the mechanical and biological properties of HUgel and favor the formation of long, highly aligned myotube bundles. Additionally, we performed in situ force measurements of electrical stimulation-induced contractions. Altogether, the results presented in this thesis provide promising approaches to advanced cell culture models of skeletal muscle tissue that could be valuable tools for fundamental studies, disease modeling, and future personalized medicine.
El músculo esquelético tiene funciones esenciales para la salud que pueden verse afectadas por enfermedades neuromusculares o metabólicas. Actualmente, la investigación fundamental y preclínica se basa en cultivos celulares en 2D y modelos animales. Sin embargo, estos ensayos tienen relevancia limitada para la salud humana. En cambio, modelos in vitro de tejidos 3D que mimeticen la arquitectura y funcionalidad del músculo esquelético, podrían complementar las estrategias 2D tradicionales. Por lo tanto, el objetivo principal de esta tesis fue desarrollar tejidos de músculo esquelético en 3D para estudios sobre el metabolismo muscular y modelos de enfermedades in vitro. Los tejidos fueron desarrollados mediante diferentes técnicas de microfabricación de hidrogeles, en los que se encapsularon células precursoras del músculo esquelético introduciendo las señales topográficas adecuadas para guiar la formación de fibras musculares. Las propiedades de estos biomateriales fueron optimizadas para garantizar su biocompatibilidad y promover la miogénesis. Estos biomateriales mantienen su estructura durante periodos de cultivo prolongados, permitiendo la formación y diferenciación de miotubos 3D altamente alineados. La función endócrina de los tejidos fue evaluada utilizando un dispositivo músculo-en-un-chip, con el que fue posible medir la liberación de citoquinas secretadas tras estimulación eléctrica o biológica. Posteriormente, se desarrolló el primer modelo 3D de músculo esquelético humano para la distrofia miotónica tipo 1. Como prueba de concepto, demostramos que el tratamiento con un oligonucleótido antisentido, antagomiR-23b, podría rescatar fenotipos moleculares y estructurales en los tejidos fabricados a partir de células de pacientes. Finalmente, se desarrollaron tejidos funcionales en cultivos celulares xeno-free, con el objetivo de incrementar la relevancia de modelos humanos en los que fue posible medir las fuerzas generada por tejidos contráctiles. En conjunto, los resultados de esta tesis proporcionan enfoques prometedores para modelos avanzados de músculo esquelético que podrían ser herramientas valiosas para estudios fundamentales, modelos de enfermedades y medicina personalizada.
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Kim, Hyeon Yu Ph D. Massachusetts Institute of Technology. "Enhancing functionalities of engineered skeletal muscle tissues by recreating natural environmental cues." Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/122138.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Mechanical Engineering, 2019
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 101-112).
Engineered skeletal muscle tissue is a three-dimensional contractile tissue made from muscle cells and the extracellular matrix (ECM). It can be used as a drug testing platform or an implantable tissue, but its practical use has been limited by inferior contractile performance and small size compared to natural muscles. This thesis aims to implement environmental cues and essential elements of natural muscles to improve the contractile performance and increase its size beyond the diffusion limit. Firstly, inspired by the observation that the natural muscles are exposed to electric potentials from neurons in combination with mechanical stretching from surrounding muscles, a new muscle training system was developed to apply coordinated electrical and mechanical stimulation.
Both the experimental results and the mechanistic model suggest the combined stimulation reorients the ECM fibers in such a way that the parallel ECM stiffness is reduced, while the serial ECM stiffness is increased, which reduces resistance to muscle contraction and increases force transmission in the engineered muscles, respectively. Secondly, large-sized natural muscles are fully vascularized so that oxygen and nutrients can be supplied. However, vascularization of the engineered skeletal muscle has been challenging because the microenvironmental requirement for differentiating myoblasts is incompatible with the one for culturing endothelial cells. In contrast, the natural muscle tissue has a compartment structure, where endothelial cells are exposed to blood plasma, while myoblasts are surrounded by interstitial fluid.
In this thesis, we modeled the natural fluid compartments by creating an in vitro perfusable vasculature running through a skeletal muscle tissue with physiologic cell density. The tissue is designed to have a coaxial tubular shape with a perfusable vasculature at the center. Through the in vitro fluid compartments, endothelial cells are exposed to endothelial cell growth medium running through the vascular channel, and the skeletal muscle cells are surrounded by muscle differentiation medium. By using this platform, engineered muscle tissue was successfully scaled up from microscale to subcentimeter scale. This platform also enabled to show that coculturing with the two separate media from an early stage of muscle differentiation leads to increased contractile force, thicker myotubes, and more muscle differentiation compared to using a single coculture medium.
Furthermore, the engineered skeletal muscles were further vascularized by inducing angiogenic sprouting from the vascular channel penetrating into the muscle tissue. This thesis will contribute to utilizing engineered skeletal muscles in practical applications with improved functionalities and provide a new model to study heterotypic cell-cell interactions in skeletal muscle tissues.
by Hyeon Yu Kim.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Mechanical Engineering
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Ciucci, Giulio. "Engineered heart tissues to investigate the role of mechanical loading and injury in cardiomyocyte proliferation." Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/312213.

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Myocardial infarction is one of the most severe acute pathologies of the cardiovascular system. The adult mammalian heart is indeed unable to regenerate most of the lost cardiomyocytes (CMs) after cardiac injury. The loss of cardiomyocytes and the myocardial scarring after myocardial infarction eventually compromise contractility of the remaining myocardium, leading to heart failure. Therefore, promoting heart regeneration is one of the most crucial therapeutic targets in cardiovascular medicine. The lack of regenerative response is due to the loss of proliferative capacity of adult CMs which in mice occurs seven days after birth. One of the events which occur at birth in neonatal hearts is a sudden increase in mechanical loading that may contribute to switching mammal CMs phenotype from neonatal proliferative to adult postmitotic. Therefore, understanding the role of mechanotransduction in regulating the balance between CM proliferation and maturation may bring us to the identification of unknown mediators and new potential strategies to induce cardiac regeneration. Regulation of mechanical load in bi-dimensional cultures of CMs can be achieved in different ways, however, the poor degree of CM maturation that can be reached in a culture dish together with the lack of a tridimensional structure represent a major limitation to performing mechanotransduction studies. In our work we developed a novel system to study mechanotransduction of CMs based on 3D culture of cardiac cells, called engineered heart tissues (EHTs), that allow us to reduce or increase mechanical loading easily. We show that the three-dimensional setting of the culture leads to an improvement of CM maturation that may be reversed by mechanical unloading inducing cell proliferation. On the other hand, a persisting overload stimulus eventually induces CM switch to a more mature phenotype with a low degree of proliferation. Also, we have focused our work on developing an EHT-based model able to recapitulate the adult infarct injury in order to investigate the biology of cardiac regeneration in this setting. Specifically, we set up a cryoinjury protocol that is relatively easy and reproducible. Cryoinjury produces a localized injury without compromising EHT’s structural integrity. Indeed, all the EHTs subjected to cryoinjury preserved their contractile activity and did not show any significant change in shape. Considering that EHTs are unpurified cardiac culture rich in fibroblast and endothelial cells, we observed that cryoinjury induce fibroblast proliferation and activation together with a lack of proliferative response of the cardiomyocytes which is, on the other hand, present in the early phase of EHT’s development, similarly to what has been shown in mice and rats after myocardial infarction, highlighting the robustness of our cryoinjury approach as a model to investigate cardiac regeneration.
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Greer, Linda S. "Material property testing of a collagen/smooth muscle cell gel for the development of a tissue engineered vascular graft." Thesis, Georgia Institute of Technology, 1994. http://hdl.handle.net/1853/33447.

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Letuffe-Brenière, David [Verfasser], and Thomas [Akademischer Betreuer] Eschenhagen. "Modelling catecholaminergic polymorphic ventricular tachycardia with patient-specific iPSC-derived engineered heart tissues / David Letuffe-Brenière. Betreuer: Thomas Eschenhagen." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2016. http://d-nb.info/1095766554/34.

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Letuffe-Brenière, David Verfasser], and Thomas [Akademischer Betreuer] [Eschenhagen. "Modelling catecholaminergic polymorphic ventricular tachycardia with patient-specific iPSC-derived engineered heart tissues / David Letuffe-Brenière. Betreuer: Thomas Eschenhagen." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2016. http://nbn-resolving.de/urn:nbn:de:gbv:18-77988.

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Levent, Elif [Verfasser], Wolfram-Hubertus [Akademischer Betreuer] Zimmermann, Dörthe [Gutachter] Katschinski, and Susanne [Gutachter] Lutz. "Characterization of cardiac progenitor cell activity in engineered heart muscle / Elif Levent. Betreuer: Wolfram-Hubertus Zimmermann. Gutachter: Dörthe Katschinski ; Susanne Lutz." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1104480476/34.

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Golat, Brian [Verfasser], Wolfram-H. [Akademischer Betreuer] Zimmermann, Rüdiger [Gutachter] Behr, Lutz [Gutachter] Walter, Ralf [Gutachter] Dressel, Stefan [Gutachter] Luther, and Steven [Gutachter] Johnsen. "Development of a Rhesus macaque engineered heart muscle model from pluripotent stem cells / Brian Golat ; Gutachter: Rüdiger Behr, Lutz Walter, Ralf Dressel, Stefan Luther, Steven Johnsen ; Betreuer: Wolfram-H. Zimmermann." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1135487715/34.

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Golat, Brian. "Development of a Rhesus macaque engineered heart muscle model from pluripotent stem cells." Doctoral thesis, 2017. http://hdl.handle.net/11858/00-1735-0000-0023-3E73-D.

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Schlick, Susanne. "Fibroblast-Cardiomyocyte Cross-Talk in Heart Muscle Formation and Function." Doctoral thesis, 2018. http://hdl.handle.net/11858/00-1735-0000-002E-E57D-3.

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Books on the topic "Engineered Heart Muscle Tissues"

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Herman, Vandenburgh, and United States. National Aeronautics and Space Administration., eds. Tissue-engineered skeletal muscle organoids for reversible gene therapy: Brief report. [Washington, DC: National Aeronautics and Space Administration, 1996.

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Wakatsuki, Tetsuro. Rapid Prototyping of Engineered Heart Tissues through Miniaturization and Phenotype-Automation. INTECH Open Access Publisher, 2011.

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1944-1988, Robinson T. F., and Kinne Rolf K. H, eds. Cardiac myocyte-connective tissue interactions in health and disease. Basel: Karger, 1990.

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

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Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will learn about bioink—a bioprinting material containing living cells and supportive biomaterials. In addition, readers will become at ease with concepts such as fugitive inks (sacrificial inks used to make channels for blood flow), extracellular matrices (the biological environment surrounding cells), decellularization (the process of isolating cells from their native environment), hydrogels (water-based substances that can substitute for the extracellular matrix), rheology (the flow properties of a bioink), and bioreactors (containers to provide the environment cells need to thrive and multiply). Further vocabulary that will become familiar includes diffusion (passive movement of oxygen and nutrients from regions of high concentration to regions of low concentration), stem cells (cells with the potential to develop into different bodily cell types), progenitor cells (early descendants of stem cells), gene expression (the process by which proteins develop from instructions in our DNA), and growth factors (substances—often proteins—that stimulate cell growth, proliferation, and differentiation). The book contains an extensive glossary for quick reference.
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Wang, Tammy, Jocelyn Wong, and Anita Honkanen. Glycogen Storage Diseases. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0048.

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Glycogen storage diseases result from deficiencies of various enzymes or proteins in the pathways of glycogen metabolism. The reduction in effective glucose storage and/or mobilization results in hypoglycemia and accumulation of glycogen in tissues. Diagnosis can occur at any age, from infancy to adulthood, depending on the pathway affected and the degree of enzyme deficiency. The clinical presentation varies, but the most commonly affected organ systems include the heart, liver, and skeletal muscles. In addition to the morbidity that can occur from dysfunction of these organs, important anesthetic implications include administration of glucose-containing fluids to avoid hypoglycemia, monitoring for acidosis, and caution with use of depolarizing muscle relaxants because of the potential risk of hyperkalemia and rhabdomyolysis. Inheritance is commonly autosomal recessive.
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van Hinsbergh, Victor W. M. Physiology of blood vessels. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0002.

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This chapter covers two major fields of the blood circulation: ‘distribution’ and ‘exchange’. After a short survey of the types of vessels, which form the circulation system together with the heart, the chapter describes how hydrostatic pressure derived from the heartbeat and vascular resistance determine the volume of blood that is locally delivered per time unit. The vascular resistance depends on the length of the vessel, blood viscosity, and, in particular, on the diameter of the vessel, as formulated in the Poiseuille-Hagen equation. Blood flow can be determined in vivo by different imaging modalities. A summary is provided of how smooth muscle cell contraction is regulated at the cellular level, and how neuronal, humoral, and paracrine factors affect smooth muscle contraction and thereby blood pressure and blood volume distribution among tissues. Subsequently the exchange of solutes and macromolecules over the capillary endothelium and the contribution of its surface layer, the glycocalyx, are discussed. After a description of the Starling equation for capillary exchange, new insights are summarized(in the so-called glycocalyx cleft model) that led to a new view on exchange along the capillary and on the contribution of oncotic pressure. Finally mechanisms are indicated in brief that play a role in keeping the blood volume constant, as a constant volume is a prerequisite for adequate functioning of the circulatory system.
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Book chapters on the topic "Engineered Heart Muscle Tissues"

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Tiburcy, Malte, Tim Meyer, Poh Loong Soong, and Wolfram-Hubertus Zimmermann. "Collagen-Based Engineered Heart Muscle." In Methods in Molecular Biology, 167–76. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1047-2_15.

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Keller, Bradley B., Fei Ye, Fangping Yuan, Hiren Trada, Joseph P. Tinney, Kevin M. Walsh, and Hidetoshi Masumoto. "Engineered Cardiac Tissues Generated from Immature Cardiac and Stem Cell-Derived Cells: Multiple Approaches and Outcomes." In Etiology and Morphogenesis of Congenital Heart Disease, 329–36. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-54628-3_46.

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Ye, Fei, Shuji Setozaki, William J. Kowalski, Marc Dwenger, Fangping Yuan, Joseph P. Tinney, Takeichiro Nakane, Hidetoshi Masumoto, and Bradley B. Keller. "Progress in the Generation of Multiple Lineage Human-iPSC-Derived 3D-Engineered Cardiac Tissues for Cardiac Repair." In Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension, 353–61. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1185-1_54.

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Bremner, Samantha, Alex J. Goldstein, Ty Higashi, and Nathan J. Sniadecki. "Engineered Heart Tissues for Contractile, Structural, and Transcriptional Assessment of Human Pluripotent Stem Cell-Derived Cardiomyocytes in a Three-Dimensional, Auxotonic Environment." In Methods in Molecular Biology, 87–97. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2261-2_6.

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Zimmermann, Wolfram-Hubertus. "Engineered Heart Muscle Models in Phenotypic Drug Screens." In Handbook of Experimental Pharmacology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/164_2020_385.

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Wakatsuki, Tetsuro. "Rapid Prototyping of Engineered Heart Tissues through Miniaturization and Phenotype-Automation." In Tissue Engineering for Tissue and Organ Regeneration. InTech, 2011. http://dx.doi.org/10.5772/21199.

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Nakano, Shintaro, Toshihiro Muramatsu, Shigeyuki Nishimura, and Takaaki Senbonmatsu. "Cardiomyocyte and Heart Failure." In Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans. InTech, 2012. http://dx.doi.org/10.5772/47772.

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G., Canan. "Role of Prokineticin in Epicardial Progenitor Cell Differentiation to Regenerate Heart." In Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans. InTech, 2012. http://dx.doi.org/10.5772/48234.

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"Cytochemical demonstration of cardiac glycosides in the heart muscle tissues using lectins and aldehydebisulfite- toluidine blue (abt) reaction." In Proceedings of the Sixth International Lectin Meeting, Poznan, Poland, September 2–6, 1984, 109–16. De Gruyter, 1985. http://dx.doi.org/10.1515/9783112322086-014.

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Hocker, Sara E., and Ali Daneshmand. "Electrolyte Disturbances and Acid-Base Imbalance." In Mayo Clinic Neurology Board Review, edited by Kelly D. Flemming, 1141–46. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197512166.003.0124.

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Electrolyte disorders are among the most common clinical problems encountered in critically ill patients. Disorders such as severe burns, trauma, sepsis, acute brain injury, and heart failure lead to disturbances in fluid and electrolyte homeostasis through complex mechanisms involving deregulation or activation of hormonal systems and ischemic or nephrotoxic kidney injury. Inappropriate fluid management should also be considered in the differential diagnosis of electrolyte disturbances in patients in intensive care units. Electrolyte imbalances produce both central and peripheral neurologic dysfunction because electrochemical membrane potentials in brain, nerve, and muscle tissues are particularly sensitive to chemical, ionic, and osmolar shifts.
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Conference papers on the topic "Engineered Heart Muscle Tissues"

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Zhang, Ting, Leo Q. Wan, Anna Marsano, Robert Maidhof, Yongnian Yan, Jiluan Pan, and Gordana Vunjak-Novakovic. "Chitosan-Collagen Based Channeled Scaffold for Cardiac Tissue Engineering." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206639.

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Tremendous efforts have been made for engineering cardiac tissue for myocardial infarction therapy [1]. Various materials and forming methods have been explored, but due to the specific physiological properties of cardiac muscle tissue, challenges still exist [2]. One of those is to create biomimetic extracellular materials to support cell function and electromechanical coupling. The scaffold material should be biocompatible, biochemically stable, mechanically strong, and highly extensible, just like native heart tissue [2]. Another challenge is to create vascular networks for oxygen and nutrient supply, much as the capillaries do in natural heart tissue [3]. In this study, chitosan and collagen were chosen to fabricate cardiac constructs with channels as small as 200 μm in diameter. Several factors such as chitosan and crosslinker concentrations and coating proteins were optimized for mechanical strength and cell seeding efficiency. Engineered tissues of significant size (12 mm in diameter × 2 mm thick) were generated in vitro using this method.
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Trubelja, Alen, John W. MacArthur, Joseph J. Sarver, Jeffrey E. Cohen, Yasuhiro Shudo, Alexander S. Fairman, Jay Patel, William Hiesinger, Pavan Atluri, and Y. Joseph Woo. "Bioengineered SDF-1a Analogue Delivered as an Angiogenic Therapy Significantly Normalizes Elastic and Viscoelastic Material Properties of Infarcted Cardiac Muscle." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14602.

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Heart disease is a leading cause of death worldwide, and coronary heart disease causes 1 of every 6 deaths in the United States [1]. Following a myocardial infarction, scar tissue gradually replaces myocardium that is lost through a process of collagen deposition and an increase in tensile strength of the tissue [2]. This leads to infarct expansion, adverse ventricular remodeling and dysfunction, and ultimately heart failure. Dilation of the left ventricle (LV) leads to increased LV wall stress and is ultimately responsible for adverse ventricular remodeling. LV dilation causes stretching and thereby increased wall stress, prohibiting cardiomyocytes from effectively contracting, which leads to further dilation, and ultimately a decrease in cardiac pump efficiency [3]. Previously, it has been shown that using a tissue filler to modify the material properties of an infarct limits the process of ventricular remodeling [4]. Angiogenesis is another mechanism by which adverse ventricular remodeling can be limited. Previously, our group developed engineered stromal cell-derived factor-1α (ESA), a computationally designed analog of an established endothelial progenitor cell chemokine, SDF-1α, and demonstrated that ESA injection enhances LV function by promoting angiogenesis and retains the native properties of the extracellular matrix (ECM) [5] [6]. In this study, we propose that injection of ESA to infarcted cardiac muscle improves the tensile strength and viscoelastic properties of ventricular muscle.
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Sacks, Michael S. "Biomechanics of engineered heart valve tissues." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.259756.

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Sacks, Michael S. "Biomechanics of Engineered Heart Valve Tissues." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4397535.

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Cox, Martijn A. J., Jeroen Kortsmit, Niels J. B. Driessen, Carlijn V. C. Bouten, and Frank P. T. Baaijens. "Inverse Mechanical Characterization of Tissue Engineered Heart Valves." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192521.

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Over the last few years, research interest in tissue engineering as an alternative for current treatment and replacement strategies for cardiovascular and heart valve diseases has significantly increased. In vitro mechanical conditioning is an essential tool for engineering strong implantable tissues [1]. Detailed knowledge of the mechanical properties of the native tissue as well as the properties of the developing engineered constructs is vital for a better understanding and control of the mechanical conditioning process. The nonlinear and anisotropic behavior of soft tissues puts high demands on their mechanical characterization. Current standards in mechanical testing of soft tissues include (multiaxial) tensile testing and indentation tests. Uniaxial tensile tests do not provide sufficient information for characterizing the full anisotropic material behavior, while biaxial tensile tests are difficult to perform, and boundary effects limit the test region to a small central portion of the tissue. In addition, characterization of the local tissue properties from a tensile test is non-trivial. Indentation tests may be used to overcome some of these limitations. Indentation tests are easy to perform and when indenter size is small relative to the tissue dimensions, local characterization is possible. We have demonstrated that by recording deformation gradients and indentation force during a spherical indentation test the anisotropic mechanical behavior of engineered cardiovascular constructs can be characterized [2]. In the current study this combined numerical-experimental approach is used on Tissue Engineered Heart Valves (TEHV).
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Karpiouk, Andrei B., Don J. VanderLaan, Kirill V. Larin, and Stanislav Y. Emelianov. "Optical coherent elastography method for stiffness assessment of heart muscle tissues (Conference Presentation)." In Optical Elastography and Tissue Biomechanics V, edited by Kirill V. Larin and David D. Sampson. SPIE, 2018. http://dx.doi.org/10.1117/12.2295762.

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Salinas, M., D. Schmidt, R. Lange, M. Libera, and S. Ramaswamy. "Computational Prediction of Fluid Induced Stress States in Dynamically Conditioned Engineered Heart Valve Tissues." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80787.

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There is extensive documented evidence that mechanical conditioning plays a significant role in the development of tissue grown in-vitro for heart valve scaffolds [1–3]. Modern custom made bioreactors have been used to study the mechanobiology of engineered heart valve tissues [1]. Specifically fluid-induced shears stress patterns may play a critical role in up-regulating extracellular matrix secretion by progenitor cell sources such as bone marrow derived stem cells (BMSCs) [2] and increasing the possibility of cell differentiation towards a heart valve phenotype. We hypothesize that specific biomimetic fluid induced shear stress environments, particularly oscillatory shear stress (OSS), have significant effects on BMSCs phenotype and formation rates. As a first step here, we attempt to quantify and delineate the entire 3-D flow field by developing a CFD model to predict the fluid induced shear stress environments on engineered heart valves tissue under quasi-static steady flow and dynamic steady flow conditions.
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Win, Zaw, Geoffrey D. Vrla, Emily N. Sevcik, and Patrick W. Alford. "Microfluidic Device for Spatial Control of Cell Seeding in Engineered Tissues." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14510.

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In vivo tissues have finely controlled hierarchical structure that is often difficult to mimic in vitro. Microfabrication techniques, such as microcontact printing, can be used to reproduce tissue structure in vitro by controlling cell shape and orientation [1]. Several recent results suggest that cellular organization and structure can influence tissue function in engineered tissues [2–4]. For example, using microcontact printing and muscular thin film technology, we recently demonstrated that engineered vascular tissues whose smooth muscle cells possessed more elongated spindle-like geometries, similar to in vivo structure, exhibited more physiological contractile function [5]. In these studies, cells were seeded using traditional imprecise seeding methods. But recent results have shown that cell-cell coupling plays a significant role in functional contractility [6], suggesting that not only cellular geometry, but cell-cell organization, within a tissue is important to reproduce in engineered tissues to mimic in vivo function.
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van Vlimmeren, Marijke A. A., Anita Driessen-Mol, Cees W. J. Oomens, and Frank P. T. Baaijens. "The Potential of Prolonged Tissue Culture to Reduce Stress Generation and Retraction in Engineered Heart Valve Tissues." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53120.

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Heart valve tissue engineering (TE) relies on extracellular matrix production by cells seeded into a degrading scaffold material. Valves are cultured constraint with the leaflets attached to each other for 4 weeks [1]. The seeded cells naturally exert traction forces to their surroundings and due to an imbalance between scaffold, tissue and these traction forces, stress is generated within the tissue, which is good for tissue formation and architecture. However, during culture it causes tissue compaction, resulting in leaflet flattening, and at time of implantation, the leaflets are separated and the generated stress causes retraction of the leaflets (fig 1). This retraction on its turn results in loss of functionality.
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Furusawa, Kazuya. "Effects of Mechanical Properties and Morphologies of Collagen Hydrogels on Tissue Hierarchical Structures of 3D Engineered Muscle Tissues." In 2019 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2019. http://dx.doi.org/10.1109/mhs48134.2019.9249284.

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Reports on the topic "Engineered Heart Muscle Tissues"

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Kanner, Joseph, Edwin Frankel, Stella Harel, and Bruce German. Grapes, Wines and By-products as Potential Sources of Antioxidants. United States Department of Agriculture, January 1995. http://dx.doi.org/10.32747/1995.7568767.bard.

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Several grape varieties and red wines were found to contain large concentration of phenolic compounds which work as antioxidant in-vitro and in-vivo. Wastes from wine production contain antioxidants in large amounts, between 2-6% on dry material basis. Red wines but also white wines were found to prevent lipid peroxidation of turkey muscle tissues stored at 5oC. The antioxidant reaction of flavonoids found in red wines against lipid peroxidation were found to depend on the structure of the molecule. Red wine flavonoids containing an orthodihydroxy structure around the B ring were found highly active against LDL and membrane lipid peroxidation. The antioxidant activity of red wine polyphenols were also found to be dependent on the catalyzer used. In the presence of H2O2-activated myoglobin, the inhibition efficiency was malvidin 3-glucoside>catechin>malvidin>resveratol. However, in the presence of an iron redox cycle catalyzer, the order of effectiveness was resveratol>malvidin 3-glucoside = malvidin>catechin. Differences in protein binding were found to affect antioxidant activity in inhibiting LDL oxidation. A model protein such as BSA, was investigated on the antioxidant activity of phenolic compounds, grape extracts, and red wines in a lecithin-liposome model system. Ferulic acid followed by malvidin and rutin were the most efficient in inhibiting both lipid and protein oxidation. Catechin, a flavonal found in red-wines in relatively high concentration was found to inhibit myoglobin catalyzed linoleate membrane lipid peroxidation at a relatively very low concentration. This effect was studied by the determination of the by-products generated from linoleate during oxidation. The study showed that hydroperoxides are catalytically broken down, not to an alcohol but most probably to a non-radical adduct. The ability of wine-phenolics to reduce iron and from complexes with metals were also demonstrated. Low concentration of wine phenolics were found to inhibit lipoxygenase type II activity. An attempt to understand the bioavailability in humans of antocyanins from red wine showed that two antocyanins from red wine were found unchanged in human urine. Other antocyanins seems to undergo molecular modification. In hypercholesterolemic hamsters, aortic lipid deposition was significantly less in animals fed diets supplemented with either catechin or vitamin E. The rate of LDL accumulation in the carotid arteries was also significantly lower in the catechin and vitamin E animal groups. These results suggested a novel mechanism by which wine phenolics are associated with decreased risk of coronary heart diseases. This study proves in part our hypothesis that the "French Paradox" could be explained by the action of the antioxidant effects of phenolic compounds found at high concentration in red wines. The results of this study argue that it is in the interest of public health to increase the consumption of dietary plant falvonoids. Our results and these from others, show that the consumption of red wine or plant derived polyphenolics can change the antioxidant tone of animal and human plasma and its isolated components towards oxidative reactions. However, we need more research to better understand bioavailability and the mechanism of how polyphenolics affect health and disease.
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Funkenstein, Bruria, and Cunming Duan. GH-IGF Axis in Sparus aurata: Possible Applications to Genetic Selection. United States Department of Agriculture, November 2000. http://dx.doi.org/10.32747/2000.7580665.bard.

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Many factors affect growth rate in fish: environmental, nutritional, genetics and endogenous (physiological) factors. Endogenous control of growth is very complex and many hormone systems are involved. Nevertheless, it is well accepted that growth hormone (GH) plays a major role in stimulating somatic growth. Although it is now clear that most, if not all, components of the GH-IGF axis exist in fish, we are still far from understanding how fish grow. In our project we used as the experimental system a marine fish, the gilthead sea bream (Sparus aurata), which inhabits lagoons along the Mediterranean and Atlantic coasts of Europe, and represents one of the most important fish species used in the mariculture industry in the Mediterranean region, including Israel. Production of Sparus is rapidly growing, however, in order for this production to stay competitive, the farming of this fish species has to intensify and become more efficient. One drawback, still, in Sparus extensive culture is that it grows relatively slow. In addition, it is now clear that growth and reproduction are physiological interrelated processes that affect each other. In particular sexual maturation (puberty) is known to be closely related to growth rate in fish as it is in mammals, indicating interactions between the somatotropic and gonadotropic axes. The goal of our project was to try to identify the rate-limiting components(s) in Sparus aurata GH-IGF system which might explain its slow growth by studying the ontogeny of growth-related genes: GH, GH receptor, IGF-I, IGF-II, IGF receptor, IGF-binding proteins (IGFBPs) and Pit-1 during early stages of development of Sparus aurata larvae from slow and fast growing lines. Our project was a continuation of a previous BARD project and could be divided into five major parts: i) obtaining additional tools to those obtained in the previous project that are necessary to carry out the developmental study; ii) the developmental expression of growth-related genes and their cellular localization; iii) tissue-specific expression and effect of GH on expression of growth-related genes; iv) possible relationship between GH gene structure, growth rate and genetic selection; v) the possible role of the IGF system in gonadal development. The major findings of our research can be summarized as follows: 1) The cDNAs (complete or partial) coding for Sparus IGFBP-2, GH receptor and Pit-1 were cloned. Sequence comparison reveals that the primary structure of IGFBP-2 protein is 43-49% identical to that of zebrafish and other vertebrates. Intensive efforts resulted in cloning a fragment of 138 nucleotides, coding for 46 amino acids in the proximal end of the intracellular domain of GH receptor. This is the first fish GH receptor cDNA that had been cloned to date. The cloned fragment will enable us to complete the GH - receptor cloning. 2) IGF-I, IGF-II, IGFBP-2, and IGF receptor transcripts were detected by RT-PCR method throughout development in unfertilized eggs, embryos, and larvae suggesting that these mRNAs are products of both the maternal and the embryonic genomes. Preliminary RT-PCR analysis suggest that GH receptor transcript is present in post-hatching larvae already on day 1. 3) IGF-1R transcripts were detected in all tissues tested by RT-PCR with highest levels in gill cartilage, skin, kidney, heart, pyloric caeca, and brain. Northern blot analysis detected IGF receptor only in gonads, brain and gill cartilage but not in muscle; GH increased slightly brain and gill cartilage IGF-1R mRNA levels. 4) IGFBP-2 transcript were detected only in liver and gonads, when analyzed by Northern blots; RT-PCR analysis revealed expression in all tissues studied, with the highest levels found in liver, skin, gonad and pyloric caeca. 5) Expression of IGF-I, IGF-II, IGF-1R and IGFBP-2 was analyzed during gonadal development. High levels of IGF-I and IGFBP-2 expression were found in bisexual young gonads, which decreased during gonadal development. Regardless of maturational stage, IGF-II levels were higher than those of IGF-L 6) The GH gene was cloned and its structure was characterized. It contains minisatellites of tandem repeats in the first and third introns that result in high level of genetic polymorphism. 7) Analysis of the presence of IGF-I and two types of IGF receptor by immunohistochemistry revealed tissue- and stage-specific expression during larval development. Immunohistochemistry also showed that IGF-I and its receptors are present in both testicular and ovarian cells. Although at this stage we are not able to pinpoint which is the rate-limiting step causing the slow growth of Sparus aurata, our project (together with the previous BARD) yielded a great number of experimental tools both DNA probes and antibodies that will enable further studies on the factors regulating growth in Sparus aurata. Our expression studies and cellular localization shed new light on the tissue and developmental expression of growth-related genes in fish.
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