Relevant bibliographies by topics / Sarcomere mechanics

Contents

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

Academic literature on the topic 'Sarcomere mechanics'

Author: Grafiati
Published: 10 March 2023
Last updated: 11 March 2023

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Journal articles on the topic "Sarcomere mechanics"

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Crocini, Claudia, and Michael Gotthardt. "Cardiac sarcomere mechanics in health and disease." Biophysical Reviews 13, no. 5 (2021): 637–52. http://dx.doi.org/10.1007/s12551-021-00840-7.

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AbstractThe sarcomere is the fundamental structural and functional unit of striated muscle and is directly responsible for most of its mechanical properties. The sarcomere generates active or contractile forces and determines the passive or elastic properties of striated muscle. In the heart, mutations in sarcomeric proteins are responsible for the majority of genetically inherited cardiomyopathies. Here, we review the major determinants of cardiac sarcomere mechanics including the key structural components that contribute to active and passive tension. We dissect the molecular and structural
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Rassier, Dilson E. "Sarcomere mechanics in striated muscles: from molecules to sarcomeres to cells." American Journal of Physiology-Cell Physiology 313, no. 2 (2017): C134—C145. http://dx.doi.org/10.1152/ajpcell.00050.2017.

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Muscle contraction is commonly associated with the cross-bridge and sliding filament theories, which have received strong support from experiments conducted over the years in different laboratories. However, there are studies that cannot be readily explained by the theories, showing 1) a plateau of the force-length relation extended beyond optimal filament overlap, and forces produced at long sarcomere lengths that are higher than those predicted by the sliding filament theory; 2) passive forces at long sarcomere lengths that can be modulated by activation and Ca2+, which changes the force-len
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Lieber, R. L. "659 SARCOMERE MECHANICS." Medicine & Science in Sports & Exercise 26, Supplement (1994): S118. http://dx.doi.org/10.1249/00005768-199405001-00661.

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Müller, Dominik, Thorben Klamt, Lara Gentemann, Alexander Heisterkamp, and Stefan Michael Klaus Kalies. "Evaluation of laser induced sarcomere micro-damage: Role of damage extent and location in cardiomyocytes." PLOS ONE 16, no. 6 (2021): e0252346. http://dx.doi.org/10.1371/journal.pone.0252346.

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Whereas it is evident that a well aligned and regular sarcomeric structure in cardiomyocytes is vital for heart function, considerably less is known about the contribution of individual elements to the mechanics of the entire cell. For instance, it is unclear whether altered Z-disc elements are the reason or the outcome of related cardiomyopathies. Therefore, it is crucial to gain more insight into this cellular organization. This study utilizes femtosecond laser-based nanosurgery to better understand sarcomeres and their repair upon damage. We investigated the influence of the extent and the
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de Tombe, Pieter P., and Henk E. D. J. ter Keurs. "Cardiac muscle mechanics: Sarcomere length matters." Journal of Molecular and Cellular Cardiology 91 (February 2016): 148–50. http://dx.doi.org/10.1016/j.yjmcc.2015.12.006.

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Russell, Robert J., Shen-Ling Xia, Richard B. Dickinson, and Tanmay P. Lele. "Sarcomere Mechanics in Capillary Endothelial Cells." Biophysical Journal 97, no. 6 (2009): 1578–85. http://dx.doi.org/10.1016/j.bpj.2009.07.017.

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Russell, Robert J., Richard B. Dickinson, and Tanmay P. Lele. "Sarcomere Mechanics in the Stress Fiber." Biophysical Journal 96, no. 3 (2009): 626a. http://dx.doi.org/10.1016/j.bpj.2008.12.3310.

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NAGORNYAK, EKATERINA, and GERALD H. POLLACK. "Connecting filament mechanics in the relaxed sarcomere." Journal of Muscle Research and Cell Motility 26, no. 6-8 (2006): 303–6. http://dx.doi.org/10.1007/s10974-005-9036-3.

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Kollár, Veronika, Dávid Szatmári, László Grama, and Miklós S. Z. Kellermayer. "Dynamic Strength of Titin's Z-Disk End." Journal of Biomedicine and Biotechnology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/838530.

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Titin is a giant filamentous protein traversing the half sarcomere of striated muscle with putative functions as diverse as providing structural template, generating elastic response, and sensing and relaying mechanical information. The Z-disk region of titin, which corresponds to the N-terminal end of the molecule, has been thought to be a hot spot for mechanosensing while also serving as anchorage for its sarcomeric attachment. Understanding the mechanics of titin's Z-disk region, particularly under the effect of binding proteins, is of great interest. Here we briefly review recent findings
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Ter Keurs, Henk E. D. J., Tsuyoshi Shinozaki, Ying Ming Zhang, et al. "Sarcomere Mechanics in Uniform and Nonuniform Cardiac Muscle." Annals of the New York Academy of Sciences 1123, no. 1 (2008): 79–95. http://dx.doi.org/10.1196/annals.1420.010.

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Dissertations / Theses on the topic "Sarcomere mechanics"

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Caruel, Matthieu. "Mechanics of Fast Force Recovery in striated muscles." Phd thesis, Ecole Polytechnique X, 2011. http://pastel.archives-ouvertes.fr/pastel-00668301.

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Cette thèse est consacrée à la modélisation de la réponse transitoire d'une fibre musculaire squelettique soumise à des sollicitations mécaniques rapides. A l'échelle du nanomètre, la fibre musculaire contient des filaments d'actine et de myosine regroupés en unités contractiles appelées "sarcomères". Le filament de myosine est un assemblage de moteurs mol ́eculaires qui, en présence d'ATP, s'attachent et se d ́etachent p ́eriodiquement au filament d'actine. Au cours de ce processus d'attachement-détachement, la myosine génère une force lors d'un changement de conformation appelé "power-stroke
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Pontén, Eva. "Tendon transfer mechanics and donor muscle properties : implications in surgical correction of upper limb muscle imbalance." Doctoral thesis, Umeå universitet, Institutionen för integrativ medicinsk biologi (IMB), 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-167.

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Tendon transfer surgery is used to improve the hand function of patients with nerve injuries, spinal cord lesions, cerebral palsy (CP), stroke, or muscle injuries. The tendon of a muscle, usually with function opposite that of the lost muscle function, is transferred to the tendon of the deficient muscle. The aim is to balance the wrist and fingers to achieve better hand function. The position, function, and length at which the donor muscle is sutured is essential for the outcome for the procedure. In these studies the significance of the transferred muscle’s morphology, length and apillarizat
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Auld, Alexander. "The Mechanisms and Function of Myonuclear Movement." Thesis, Boston College, 2018. http://hdl.handle.net/2345/bc-ir:108147.

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Thesis advisor: Eric S. Folker<br>Thesis advisor: David R. Burgess<br>During muscle development, myonuclei undergo a complex set of movements that result in evenly spaced nuclei throughout the muscle cell. In many muscle diseases mispositioned myonuclei have been used as a hallmark phenotype of disease. A number of studies over the last decade have started to piece together the cytoskeletal elements that govern these movements. In Drosophila, two separate pools of Kinesin and Dynein work in synchrony to drive nuclear movement. However, it is still not clear how these two pools of microtubule m
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Pappas, Christopher Theodore. "Elucidating the Mechanisms by Which Nebulin Regulates Thin Filament Assembly in Skeletal Muscle." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/145422.

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Proper contraction of striated muscle requires the assembly of actin filaments with precise spacing, polarity and lengths, however the mechanisms by which the cell accomplishes this remain unclear. In one model, the giant protein nebulin is proposed to function as a "molecular ruler" specifying the final lengths of the actin filaments. This dissertation focuses on determining the mechanisms by which nebulin regulates thin filament assembly. We found that nebulin physically interacts with CapZ, a protein that caps the barbed end of the actin filament within the Z-disc. Reduction of nebulin
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Bohman, Lova. "Pathological Mechanisms of Sarcomere Mutations in the Disease Hypertrophic Cardiomyopathy : A Review." Thesis, Linköpings universitet, Institutionen för fysik, kemi och biologi, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-176045.

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Hypertrophic cardiomyopathy is a heart disease that is characterized by an enlarged heart muscle. Mutations to sarcomere proteins in the muscle fibers give rise to the disease, and this review aims to compile the mechanisms by which the mutations cause the disease phenotype. β-myosin heavy chain mutants affect the thick filament structure and contraction velocity of the muscle. Mutations to the myosin-binding protein C produces truncated proteins with decreased expression in the cells. Troponin T mutants cause myofibrillar disarray, alters affinity to α-tropomyosin, and are linked to a higher
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Pontén, Eva. "Tendon transfer mechanics and donor muscle properties : implications in surgical correction of upper limb muscle imbalance /." Umeå : Integrativ medicinsk biologi, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-167.

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McCain, Megan Laura. "From Womb to Doom: Mechanical Regulation of Cardiac Tissue Assembly in Morphogenesis and Pathogenesis." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10260.

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The assembly, form, and function of the heart is regulated by complex mechanical signals originating from intrinsic and extrinsic sources, such as the cytoskeleton and the extracellular matrix. During development, mechanical forces influence the self-assembly of highly organized ventricular myocardium. However, mechanical overload induces maladaptive remodeling of tissue structure and eventual failure. Thus, mechanical forces potentiate physiological or pathological remodeling, depending on factors such as frequency and magnitude. We hypothesized that mechanical stimuli in the form of microenv
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Kronbauer, Gláucia Andreza. "Características mecânicas e histológicas do músculo sóleo de ratos submetidos a treinamento de esteira em aclive e declive." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2009. http://hdl.handle.net/10183/18773.

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A literatura refere que os estímulos produzidos pelos diferentes tipos de contração no sistema músculo-esquelético geram adaptações específicas. A locomoção em aclive e declive vem sendo utilizada como modelo de treinamento concêntrico e excêntrico para estudos dessas adaptações em animais. Sendo assim este estudo teve o objetivo de avaliar características mecânicas e histológicas do músculo sóleo de ratos submetidos a treinamento em aclive ou declive. Foram avaliados 36 ratos Wistar machos (90 dias de idade no início do treinamento) divididos igualmente em três grupos: aclive (A), declive (D)
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Mouton, Jacoba Martina. "The role of novel protein-protein interactions in the function and mechanism of the sarcomeric protein, myosin binding protein H (MyBPH)." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86751.

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Thesis (PhD)--Stellenbosch University, 2014.<br>ENGLISH ABSTRACT: Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity and mortality, and is a feature of common diseases, such as hypertension and diabetes. It is therefore vital to understand the underlying mechanisms influencing its development. However, investigating the mechanisms underlying LVH in such complex disorders can be challenging. For this reason, many researchers have focused their attention on the autosomal dominant cardiac muscle disorder, hypertrophic cardiomyopathy (HCM), since it is considere
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Squarci, Caterina. "The structural dynamics of titin in situ and its role in contraction and relaxation of the striated muscle." Doctoral thesis, 2021. http://hdl.handle.net/2158/1238953.

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The aim of this work is to define the function of I-band titin as a dynamic element in parallel whit the array of myosin motors using fast half-sarcomere level mechanics on intact fibres of frog muscle in the presence of 20 uM para-nitro-blebbistatin (PNB)
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Book chapters on the topic "Sarcomere mechanics"

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Iwazumi, Tatsuo. "Mechanics of the Sarcomere." In Cardiac Mechanics and Function in the Normal and Diseased Heart. Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-67957-8_2.

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Napiwocki, Brett N., Max R. Salick, Randolph S. Ashton, and Wendy C. Crone. "Polydimethylsiloxane Lanes Enhance Sarcomere Organization in Human ESC-Derived Cardiomyocytes." In Mechanics of Biological Systems and Materials, Volume 6. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-21455-9_12.

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Thompson, Brian R., Michelle L. Asp, and Joseph M. Metzger. "Molecular Mechanism of Sarcomeric Cardiomyopathies." In Congestive Heart Failure and Cardiac Transplantation. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-44577-9_10.

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Squire, John M., Pradeep K. Luther, and Edward P. Morris. "Organisation and Properties of the Striated Muscle Sarcomere." In Molecular Mechanisms in Muscular Contraction. Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-09814-9_1.

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Trombitás, Károly, and Gerald H. Pollack. "Elastic Properties of Connecting Filaments Along the Sarcomere." In Mechanism of Myofilament Sliding in Muscle Contraction. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2872-2_7.

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ter Keurs, Henk EDJ, and Pieter P. de Tombe. "Determinants of Velocity of Sarcomere Shortening in Mammalian Myocardium." In Mechanism of Myofilament Sliding in Muscle Contraction. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2872-2_58.

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Ehler, Elisabeth, and Jean-Claude Perriard. "Emergence of the First Myofibrils and Targeting Mechanisms Directing Sarcomere Assembly in Developing Cardiomyocytes." In Myofibrillogenesis. Birkhäuser Boston, 2002. http://dx.doi.org/10.1007/978-1-4612-0199-1_3.

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"Sarcomeric Proteins in LGM D." In Molecular Mechanisms of Muscular Dystrophies. CRC Press, 2006. http://dx.doi.org/10.1201/9781498713962-16.

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Arnar, David O., and Hilma Holm. "Mechanisms of atrial fibrillation: genetics." In ESC CardioMed. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0497.

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While atrial fibrillation (AF) is common and has serious consequences, a lot is yet unknown about the causative factors underlying this arrhythmia. The role of genetics in the development of AF has become more evident in the past decade. Family history is now a firmly established risk factor and many common and rare sequence variants linked to AF have been identified. Genome-wide association studies have identified common sequence variants that associate with AF, including variants on chromosomes 4q25, 16q22, and 1q22. Nevertheless, it has become apparent that despite these findings, a substantial fraction of heritability of most complex traits remained unaccounted for. This raises the possibility that development of AF is determined by the combination of common and rare susceptibility variants. Whole genome sequencing is the most comprehensive method to analyse individual genetic variation. A paradigm shift from microarray-based genotyping studies to whole exome and whole genome sequencing is ongoing. Whole genome sequencing studies have shown mutations in myosin genes may be associated with AF, implying that variants encoding sarcomere genes may be involved in the development of this arrhythmia. While some of the sequence variants discovered suggest novel mechanisms in the pathophysiology of this complex arrhythmia, much work is still needed to fully understand the mechanisms linking many of these loci to AF. Likewise, the current clinical applicability of this information is still unclear. However, further developments in this field are expected to add to our understanding of this complex arrhythmia and hopefully lead to new therapeutic possibilities.
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Lazzeroni, Davide, and Claudio Stefano Centorbi. "Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Diagnosis, Clinical Course and Therapy." In Cardiomyopathy - Disease of the Heart Muscle [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97033.

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Hypertrophic cardiomyopathy (HCM) is a genetic disorder of cardiac myocytes that is characterized by cardiac hypertrophy, unexplained by the loading conditions, a non-dilated left ventricle and a normal or increased left ventricular ejection fraction (LV-EF). Prevalence of HCM has been estimated at 0.16% to 0.29% (≈ 1:625–1:344 individuals) in the general adult population. HCM represents the most common genetic heart disease and represent an archetypical single gene disorder with an autosomal dominant pattern of inheritance and historically termed a “disease of the sarcomere”. The precise mechanisms by which sarcomere variants result in the clinical phenotype have not been fully understood. Mutant sarcomere genes trigger several myocardial changes, leading to hypertrophy and fibrosis, which ultimately result in a small, stiff ventricle with impaired systolic and diastolic performance despite a preserved LV-EF. The most common differential diagnosis challenges in the presence of hypertrophic heart disease are represented by: athlete’s heart, hypertensive heart and other cardiomyopathies mimicking HCM. A multimodality approach using ECG, echocardiography, CMR, cardiac computed tomography (CCT) and cardiac nuclear imaging provides unique information about diagnosis, staging and clinical profiles, anatomical and functional assessment, metabolic evaluation, monitoring of treatment, follow-up, prognosis and risk stratification, as well as preclinical screening and differential diagnosis. HCM may be associated with a normal life expectancy and a very stable clinical course. However, about a third of patients develop heart failure (HF); in addition, 5–15% of cases show progression to either the restrictive or the dilated hypokinetic evolution of HCM, both of which may require evaluation for cardiac transplantation. The clinical course of HCM has been classified into four clinical stages: non-hypertrophic, classic, adverse remodeling and overt dysfunction phenotype. No evidence-based treatments are available for non-hypertrophic HCM patients (pre-hypertrophic stage), on the other hand in classic HCM, adverse remodeling and overt dysfunction phenotype, pharmacological or interventional strategies have the target to improve functional capacity, reduce symptoms, prevent disease progression. Therapeutic approach mainly differs on the basis of the presence or absence of significant obstructive HCM. Adult patients with HCM report an annual incidence for cardiovascular death of 1–2%, with sudden cardiac death (SCD), HF and thromboembolism being the main causes of death; the most commonly recorded fatal arrhythmic event is spontaneous ventricular fibrillation. For this reason, SCD risk estimation is an integral part of clinical management of HCM. International guidelines suggest the evaluation of several risk factor for SCD based on personal and family history, non-invasive testing including echocardiography, ambulatory electrocardiographic 24 hours monitoring and CMR imaging in order to identity those patients most likely to benefit implantable cardioverter-defibrillator (ICD) implantation. The present chapter summarize genetics, pathogenesis, diagnosis, clinical course and therapy of HCM as well as novel therapeutic options.
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Conference papers on the topic "Sarcomere mechanics"

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LUMENS, JOOST, TAMMO DELHAAS, BORUT KIRN, and THEO ARTS. "MODELING VENTRICULAR INTERACTION: A MULTISCALE APPROACH FROM SARCOMERE MECHANICS TO CARDIOVASCULAR SYSTEM HEMODYNAMICS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812776136_0037.

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Lin, D., and W. C. Hunter. "Method to orient cardiac tissue specimens for uniaxial mechanical testing with long axis parallel to sarcomeres." In 2011 37th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2011. http://dx.doi.org/10.1109/nebc.2011.5778647.

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Hsu, Hui-Ju, Andrea Locke, Susan Q. Vanderzyl, and Roland Kaunas. "Stretch-Induced Stress Fiber Remodeling and MAPK Activations Depend on Mechanical Strain Rate." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53464.

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Actin stress fibers (SFs), bundles of actin filaments crosslinked by α-actinin and myosin II in non-muscle cells, are mechanosensitive structural elements that respond to applied stress and strain to regulate cell morphology, signal transduction and cell function. Results from various studies indicate that myosin-generated contraction extends SFs beyond their unloaded lengths and cells maintain fiber strain at an optimal level that depends on actomyosin activity (Lu et al., 2008). Stretching the matrix upon which cells adhere perturbs the cell-matrix traction forces and cells respond by active
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Bryan, Andrea, Amy Sung, Ian Lian, and Jeffrey Omens. "The Role of Tropomodulin in Cardiac Function and Remodeling." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61363.

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Tropomodulin is an actin-capping protein in cardiac muscle, and is associated with both sarcomeric and cytoskeletal actin filaments. Homozygous knockout of erythrocyte tropomodulin (E-Tmod) is embryonically lethal, but heterozygous knockout (+/-) mice survive. Heterozygous E-Tmod knockout resulted in smaller right ventricle (RV) cavities and free walls compared to wild type. To investigate the effect of heterozygous tropomodulin knockout on mouse cardiac function and remodeling, mice (n=6 to 9) were subjected to 5 weeks of hypoxia to increase loading conditions on the RV via pulmonary hyperten
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Wei, Ailin, Zhonghai Wang, Zongming Yang, et al. "Study of the sarcomeric addition process in a tissue-like cell construct under mechanical overload via TPEF-SHG imaging system." In Multiphoton Microscopy in the Biomedical Sciences XX, edited by Ammasi Periasamy, Peter T. So, and Karsten König. SPIE, 2020. http://dx.doi.org/10.1117/12.2546280.

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Kidambi, Narayanan, R. L. Harne, and K. W. Wang. "Strain Energy Trapping due to Energetic Asymmetry in Modular Structures Inspired by Muscle Cross-Bridges." In ASME 2016 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/detc2016-59556.

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The remarkable energetic versatility and adaptability of skeletal muscle provides great inspiration to develop advanced adaptive structures and materials. These notable properties may arise from the assembly of skeletal muscle’s nanoscale cross-bridges into microscale structures known as sarcomeres. Essential understanding of muscle energetics has been developed from models of the micro/nanoscale constituents which incorporate an intriguing, asymmetric, bistable potential energy landscape to capture trends in the experimental data on cross-bridge power stroke motions. Inspired by the capabilit
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