Дисертації: "Striated"

1

North, Alison Jane. "Spectrin localisation in mammalian striated muscle." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276872.

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2

Palmer, Roy Emmet. "Striated muscle relaxation : a caged compound study." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315026.

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3

Hallett, Peter C. "Scanning force microscopy of striated muscle proteins." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296600.

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4

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". Ses caractéristiques peuvent être étudiées lors de la réponse transitoire de la fibre soumise à des sollicitations mécaniques rapides. Nous proposons un modèle mécanique innovant du demi-sarcomere permettant de relier les caractéristiques de la myosine à la réponse de la fibre complète. A la différence des modèles existants, privilégiant une approche discrète, ce modèle s'appuie sur la définition d'un potentiel d'énergie continu qui prend en compte une interaction de champ moyen entre les moteurs moléculaires. Ce système présente des réponses radicallement différentes à longueur imposée et à force imposée. Nous proposons en particulier une explication à la différence de cinétique observée expérimentalement. Nous montrons également que le demi-sarcomere est m ́ecaniquement instable ce qui explique les inhomogénéités de longueurs observées dans une myofibrille.

5

Ankrett, Richard Joseph. "Conformers of myosin from scallop striated adductor muscle." Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/35712.

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Myosin from the striated adductor muscle of scallop (Pecten maximus) folds into a compact 10S conformer, as has been characterized for smooth muscle and non-muscle myosins. The 10S conformer of scallop myosin is favoured at physiological ionic strengths in the absence of Ca2+ and in the presence of nucleotide triphoshate. The folded transition is accompanied by the trapping of the nucleotide at the active site to give a species with a half-time of about an hour at 20C. Ca2+ binding to the specific, regulatory sites on a myosin head promotes unfolding to the extended 6S conformer and activates product release by around 60-fold. The unfolding transition, however, remains much slower than the contraction-relaxation cycle of scallop striated muscle and could not play a role in the regulation of these events. The turnover of nucleotide by the 10S conformer is an order of magnitude slower than the turnover by native scallop filaments. The latter have very similar kinetic properties to that of scallop heavy meromyosin suggesting that the myosin-linked regulatory system requires only the head and neck domain to function properly. Thus there is no evidence, from nucleotide turnover measurements, for an intermolecular interaction occurring between the neck and tail regions of neighbouring myosin in the filament equivalent to that observed as an intramolecular interaction in the 10S conformer. The role of the 10S conformer in striated muscle may therefore be associated with events which occur on a slower time-scale than the contraction-relaxation cycle, such as transport of myosin molecules from their site of synthesis to the myofibril during growth and development of the muscle. Removal of either one or both of the regulatory light chains from scallop myosin prevents, or at least disfavours, formation of the folded 10S conformer. Readdition of the native regulatory light chains, or those from other other molluscan species, restores to the myosin its ability to fold. Labelling the reactive heavy chain thiol of myosin also disfavours formation of the 10S conformer and allows separation of the modified protein from the native molecules.

6

Ochmann, Constanze. "Investigating the role of Klhl31 in striated muscle." Thesis, University of East Anglia, 2013. https://ueaeprints.uea.ac.uk/45561/.

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Members of the Kelch-like family display various functions at the cellular level, such as being involved in signalling pathways, as mediators of cytoskeletal changes and most prominently by targeting specific substrates for proteasomal degradation. Previous studies suggested a role for Kelch-like 31 (Klhl31) during myogenesis, as its expression is dependent on signals responsible for the induction of myogenesis in the somites and is slightly delayed compared to the expression of early myogenic regulatory factors. With this study we wanted to analyse the function of Klhl31 during myogenesis in more detail. Using C2C12 mouse myotubes as our model cell line to study myogenic differentiation and myofibrillogenesis, we found that Klhl31 is closely associated with Actin fibres in differentiated, multi-nucleated myotubes and that observed co-localisation can be linked to C2C12 differentiation. Furthermore, we used a Yeast-2-Hybrid screen approach and GST-pull downs to find interaction partners for Klhl31. Putative interacting proteins for Klhl31 were analysed and found to be structural components of the sarcomere with many of them also being involved in myofibrillogenesis, such as Nebulin, Actin, CapZ and tropomyosin. We also analysed a possible role of Klhl31 in proteasomal degradation, as Klhl31 was shown to negatively regulate canonical Wnt-signalling. We gathered evidence that Klhl31 might interact with components of E3-Ubiquitin ligase complexes and might target specific substrates including itself for degradation by the 26S proteasome. Furthermore, we analysed the expression of Klhl31 during heart development in chick embryos, where it was restricted to the myocardium. We concluded that Klhl31 might be important during myofibrillogenesis in striated muscles. A role for Klhl31 in mature muscle might involve providing structural stabilisation in sarcomeres and during muscle contraction.

7

Schuster, Joseph M. "The contribution of titin to striated muscle shortening." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/5758.

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Thesis (M.S.)--University of Missouri-Columbia, 2008.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. "December 2008" Includes bibliographical references.

8

Briggs, Dustin L. "NATURALLY STRIATED MUSCLE: EXAMINING THE IDEOGRAPHIC CRYSTALLIZATION OF." OpenSIUC, 2016. https://opensiuc.lib.siu.edu/dissertations/1161.

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In U.S. America and much of the Western world, natural is a venerated symbolic placeholder for any number of assumed virtues and ideals. Present conflicts have brought forward questions about what natural (which I argue functions as an ideograph) should mean in contexts that seem to call for a formal, enforceable definition. In this study, I use the vocabulary of Deleuze and Guattari (1987) and the context of bodybuilding to work towards a theory of how ambiguous ideographs become "striated" or “crystallized.” Within this discussion I present instances where natural has been employed as a vehicle to cause harm, and I offer an advisement to rhetorical scholars on how we might approach striated ideographs in the future.

9

Essackjee, Hafejee Cassim. "The influence of contraction, pH and enzyme inhibition on the release of adenosine from rat gracilis muscle." Thesis, Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20565914.

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10

Rogers, Brendan James. "Arrangement and structure of α-actinins in striated muscle". Thesis, University of Leeds, 2018. http://etheses.whiterose.ac.uk/22905/.

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The smallest contractile unit within striated muscle cells are called sarcomeres. The boundary regions between sarcomeres are called Z-discs, which contain over 30 different proteins, organised within a narrow ~100 nm wide structure. Standard fluorescence microscopy approaches do not reveal the arrangement of Z-disc proteins, as the width of the Z-disc is below the resolution limit (~250 nm). The arrangement of the actin filaments and the cross-linking proteins α-actinin in the Z-discs are well characterised by electron microscopy (EM) studies, however other Z-disc proteins are not. With the development of super-resolution fluorescence microscopy techniques, it is now possible to obtain Z-disc protein localisation information. Here, dSTORM (direct Stochastic Optical Reconstruction Microscopy) was used, to investigate the arrangement of α-actinins in Z-discs of cardiomyocytes, and then the arrangement of the N-terminal ends of the giant protein titin in the Z-discs. Affimers were generated to bind α-actinin 2 and the N-terminal titin domains (Z1/Z2), to use as binders in dSTORM. Affimers are small (~12 kDa) non-antibody binding proteins, about 1/10th the size of antibodies, that can be selected to bind to a specific protein. The localisation data of dSTORM using the Affimer binders showed the same regular arrangement of α-actinins observed in EM studies. The use of dSTORM with Affimers also suggests the titin Z1/Z2 domains do not only localise at the edges of the Z-discs but arranged throughout the Z-disc with regular spacing (~25 nm) in the transverse plane of the Z-discs. Also, three mutations located in the actin binding domain of α-actinin 2 associated to hypertrophic cardiomyocytes (G111V, A119T and M228T) were characterised by in vitro co-sedimentation assays with actin. The mutants G111V and A119T did not show a significant difference in binding affinity to actin compared to the wild-type. The co-sedimentation assays did however suggest the mutation M228T significantly increases the binding affinity of α-actinin 2.

11

Chuang, Chia-Chen. "Characterization of Reperfusion Injury-Induced ROS in Striated Muscles." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1500479949278294.

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12

Huo, Jiuzhou. "Regulation of Mitochondrial Calcium Dynamics in Striated Muscle Function." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1595846761184679.

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13

Dwyer, Joseph. "Characterisation of the formin protein FHOD1 in striated muscle." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/characterisation-of-the-formin-protein-fhod1-in-striated-muscle(317eb5ca-2e74-4c63-8c45-7c96f9a3a23d).html.

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Formin homology 2 domain containing protein 1 (FHOD1) is a diaphanous related formin of the FHOD subclass. In a similar manner to other formins, FHOD1 has primarily been found to regulate the polymerisation of actin-based structures in cells. In muscle, actin is a major constituent of both skeletal and cardiac myocytes, with the thin filament system of sarcomeres and the cytoskeleton being partly composed of actin. FHOD proteins have previously been highlighted as important regulators of muscle cell biology since FHOD3, a close relative of FHOD1 was shown to be essential for myofibrillar maintenance. There is little known about the regulation of actin-based structures in muscle cells. We therefore aimed to characterise FHOD1 and probe into its involvement in myofibrillar and cytoskeletal regulation. In this study of FHOD1 we addressed various aspects of the protein including its expression pattern and localisation, function, regulation, and novel interacting partners. Insight into the expression pattern of FHOD1 was gained by examining relative protein levels in different tissues, including both healthy and diseased heart. Subcellular localisation was addressed in a number of fluorescence microscopy experiments through antibody localisation studies in muscle tissue and cultured cells and through transient transfection of GFP tagged constructs. Expression of GFP tagged fragments and mutants helped to delineate the functional distribution of the FHOD1 molecule in cells. The function of the protein was further probed via molecular knockdown by RNAi and by looking at the capacity of FHOD1 to polymerise actin in cells. The role of formins in the heart was more broadly addressed by drug inhibition of their actin polymerising capacity. Previous studies have suggested that the Rho family of small GTPases as well as the Src kinases regulate FHOD1. Involvement of the GTPases and Src was shown through biochemical experiments. Finally, a number of Yeast2Hybrid assays were performed using different domains of FHOD1 to screen for novel binding partners. Our findings would suggest that FHOD1 is a crucial regulator of the myofibrillar apparatus and the cytoskeleton at the level of actin in striated muscle.

14

Wang, Zai, and 王在. "Kinesin-1 in skeletal muscle." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41757877.

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15

Wang, Zai. "Kinesin-1 in skeletal muscle." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41757877.

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16

Burgoyne, Thomas. "Analysing the lattice transition of thin filaments in striated muscle." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5559.

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Thin filaments, through interaction with thick filaments, form the contractile apparatus of striated muscle. Therefore, the length and arrangement of the thin filaments are of key importance to the function of the muscle. The thin filaments from adjacent sarcomeres are anchored at the Z-disc. In 1968 Pringle predicted that thin filament are organised in the Z-disc in a rhomboid lattice rather than a square lattice. Previous experimental evidence has been insufficient to verify Pringle’s suggestion. In the A-band the thin filaments interdigitate with the thick filaments on a hexagonal lattice, hence from the Z-disc to the A-band, there is a transition of the lattice from square to hexagonal. In this project, I have firstly used Fourier analysis and electron tomography to investigate the thin filament lattice in the Z-disc. I have used electron tomography to determine how the lattice transition occurs between the Z-disc and the A-band. Electron tomography of these samples also allowed me to determine the lengths of thin filaments, showing unequivocally that they are of variable lengths in cardiac muscle.

17

Watson, Rachel Anne. "The role of Akt2 in skeletal muscle." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607970.

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18

Wood, Stephanie Ann Cardinal Trevor R. "A morphological and hemodynamic analysis of skeletal muscle vasculature : a thesis /." [San Luis Obispo, Calif. : California Polytechnic State University], 2008. http://digitalcommons.calpoly.edu/theses/16/.

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Thesis (M.S.)--California Polytechnic State University, 2008.
"July 2008." "In partial fulfillment of the requirements for the degree [of] Master of Science in Engineering with a specialization in Biomedical Engineering." "Presented to the faculty of California Polytechnic State University, San Luis Obispo." Major professor: Trevor Cardinal, Ph.D. Includes bibliographical references (leaves 96-101). Also available on microfiche and online.

19

Salva, Maja Zavaljevski. "Transcriptional regulation : applications toward rAAV-based gene therapies in striated muscle /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8030.

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20

Leary, Scot C. "Interactions between bioenergetics and cytochrome c oxidase levels in striated muscles." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ63432.pdf.

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21

Shaw, Christian A. "An investigation of the Coxsackie and Adenovirus Receptor in striated muscle /." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111881.

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Since its identification in 1997 as the common receptor for Coxsackie and adenovirus (CAR) multiple lines of evidence argue in favor of CAR contributing to aspects of cell adhesion in addition to serving as a viral receptor. Nevertheless, a precise biological role for CAR remains to be identified suggesting the receptor may participate in a variety of cellular functions that reflect its tissue specific and developmentally regulated expression. This thesis elucidates aspects of CAR biology in mature striated muscle by providing studies that encompass (i) its physiological cellular/subcellular localization and expression in mature striated muscle (ii) its expression profile in human diseased skeletal muscle and (iii) the potential consequences of its sustained expression in mature striated muscle where its levels would otherwise be highly attenuated.
In non-diseased, mature striated muscle despite low and barely detectable levels of the CAR transcript (cardiac and skeletal muscle respectively), we identified CAR as a novel component of the neuromuscular junction and showed its expression to be isoform-specific in contrast to the intercalated discs, where both predominant CAR isoforms are detected. We then investigated the expression of CAR at the level of human skeletal muscle disease. From these studies we observed that in diseases characterized by active necrosis and regeneration, extrasynaptic CAR expression is detectable in regenerating fibers and co-expressed with other previously described markers of regeneration at a high degree of coincidence. Moreover, extrasynaptic CAR expression appears to be a highly reliable indicator of the regenerative process offering potential use at the diagnostic level. Following these investigations, our final studies involved assessing whether sustained CAR expression might affect the normal homeostasis in skeletal and cardiac muscle using a transgenic mouse model. We discovered that transgenic mice expressing sustained high levels of CAR (as seen in the CAR+/+ transgenics) develop a lethal necrotizing myopathy characterized by dual deficiencies in dystrophin and dysferlin, two proteins pivotal in maintaining plasmalemmal integrity, raising the possibility for a previously unrecognized cause of skeletal muscle dysfunction.
Collectively these findings argue that in non-diseased mature skeletal and cardiac muscle, CAR expression is restricted to the neuromuscular junction and cardiac intercalated discs but in diseases of skeletal muscle characterized by active necrosis and regeneration, extrasynaptic CAR expression is reexpressed at these sites of injury/repair. In addition they raise the possibility that sustained CAR expression in mature skeletal muscle may be associated with altered muscle homeostasis.

22

Gibbs, Linda. "Characterisation of a porcine striated muscle myosin heavy chain genomic clone." Thesis, Royal Veterinary College (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300545.

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23

Barisic, Dominik [Verfasser], and Melanie L. [Akademischer Betreuer] Hart. "Differentiation potential of adult human MSCs into neuro-striated muscle cells." Freiburg : Universität, 2018. http://d-nb.info/1226091318/34.

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24

Salim, Oday. "Unravelling the structure of striated muscle M-band by electron tomography." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9559.

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The sarcomeric M-band in vertebrate striated muscle is thought to maintain the uniform hexagonal lattice of the thick filaments by crosslinking neighbouring thick filaments in the middle of the A-band. It is also thought to maintain the fine axial alignment of the thick filaments within the A-band. The M-band has been implicated with fundamental signalling complexes that control sarcomeric protein turnover during development. There are two classes of M-band: 3-line M-band, which has a prominent central M1 stripe; and 2- line M-band that lacks the central M1 stripe. The aim of this study is to examine the ultrastructure of the different M-band types using electron microscopy and tomography. The 3-line M-band was examined thoroughly using electron microscopy and tomography of longitudinal and transverse sections. Profile plot analysis of longitudinal section micrographs and tomograms showed that the peaks of the M-band were found to be associated with protrusions on the thick filaments, rather than the M-bridges. Thus the M-bridges only contribute to the background density of the profile (envelope function) rather than the peaks. Analysis of transverse section tomograms unravelled new structural details of the M-band, which allowed us to model the possible pathways of M-band proteins. Projection of our model into longitudinal section view shows that the M-band appearance is a projection effect of the underlying 3D structure. Examination of the thick filament backbone structure showed that it is rotating at the bare region and the M-band, which suggested that the thick filament may have torsional flexibility. The path of titin in the A-band is thought to run along the thick filament in the crossbridge region, but it is not known whether titin is dislodged from the thick filament at the M-region or not. We find evidence (from the 3-line M-band specimen) that titin could be dislodged from the thick filament at the periphery of the M-region. We speculate that titin may exist as a doublet along the crossbridge segment and splits into single filaments after dislodging at the M-region. For the 2-line M-band study, freshly dissected bony fish heart muscle was prepared for plastic embedding. In longitudinal sections, the M-band did not show clear stripes but the average profile plot showed clear M-band peaks that lack the central M1 peak. Transverse sections of the M-band did not show clear hexagonal network of M-bridges. In addition, thick filaments orientations and the thick filament lattice were less ordered than in the 3-line M-band muscle. Modelling a thick filament from the raw tomograms shows a backbone structure similar to the 3-line M-band; a novel M-band model was produced, where the M-bridges originating at M4 (and M4’) do not cross the central M1 line but are oriented outwards towards the bare region. We hypothesise that M-protein is responsible for the crystalline appearance of the M-band and the thick filaments in 3-line M-bands. The work carried out in this PhD investigation will help our understanding of the structural role of the M-band in different muscles. It gives the most detailed view to date of the M-band in fast, slow and cardiac muscle. It will help our understanding of the structural changes in the M-band during activation that may initiate signalling events.

25

Allhouse, Leanne Dawn. "Characterisation of troponin C, the calcium binding protein of barnacle striated muscle." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312246.

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26

Polack, Christopher [Verfasser]. "Function of Titin in Striated Muscles in Health and Disease / Christopher Polack." Berlin : Freie Universität Berlin, 2015. http://d-nb.info/108017110X/34.

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27

Van, Lehn Reid Chi. "Modeling the reaction mechanism of membrane penetration by striated amphiphitic gold nanoparticles." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/58449.

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Thesis (S.B.)--Massachusetts Institute of Technology, Dept. of Materials Science and Engineering, 2009.
Cataloged from PDF version of thesis.
Includes bibliographical references (p. 37-38).
The desire to desire targeted drug delivery devices capable of releasing therapeutic payloads within the cytosol of cells has led to research on nanoparticles as suitable drug carriers. Recently, it was shown that gold nanoparticles coated in striped, alternating layers of hydrophobic and hydrophilic ligands are capable of non-disruptively penetrating a lipid bilayer, a discovery with potential implications in drug delivery. While the reaction mechanism is not known, initial experimental results indicate that endocytosis and membrane poration could be ruled as possible mechanisms. In this work, we explore the reaction mechanism of membrane penetration using a coarse-grained Brownian Dynamics model. We also define a Monte Carlo simulation for modeling ligand motion on the nanoparticle surface based on a single order parameter, and describe a method for approximating the interaction energy with the bilayer as a function of this parameter. Our simulations demonstrate the dependence of nanoparticles penetration on the surface mobility, not explicit conformation, of coated ligands. They demonstrate that while nanoparticles with static ligands in a striped conformation are unable to penetrate the bilayer, enabling surface mobility allows penetration by the induced formation of a small, transient pore of a comparable size to the nanoparticle. Our results offer an enhanced understanding of the nanoparticles-bilayer interaction and an identification of the property necessary for membrane penetration.
by Reid Chi Van Lehn.
S.B.

28

Nicolas, Hannah Almira. "Understanding Molecular Mechanisms of Striated Muscle Laminopathies Using Cellular and Zebrafish Models." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41008.

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29

Johnson, Eric K. "A new model for the dystrophin associated protein complex in striated muscles." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354554580.

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30

Whitman, Samantha. "Fragile X Related Protein-1 (FXR1) Regulates RNA Metabolism in Striated Muscle." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/195153.

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Cardiac muscle function necessitates the meticulous assembly and interactions of several cytoskeletal and regulatory proteins into specialized structures that orchestrate contraction and transmission forces. Despite extensive studies identifying the protein components responsible for these important aspects of heart development, putative RNA based mechanisms remain poorly understood, even with their demonstrated importance in other tissues. Evidence suggests that post-transcriptional regulation is critical for muscle function, but the molecular players involved (RNA binding proteins and mRNA targets) have remained elusive. We investigated the molecular mechanisms and targets of the muscle-specific Fragile X Related protein-1 (FXR1), an RNA binding protein whose absence leads to perinatal lethality in mice. Loss of FXR1 results in global protein level alterations. Morphological and biochemical analyses of Fxr1^(-/-) mice revealed severe disruption of intercalated disc and costamere architecture and composition. We identified several candidate mRNAs specifically enriched in the FXR1 protein complex. Two targets that likely contribute to the architectural defects are desmoplakin (dsp) and talin2 (tln2). In vitro assays indicate that FXR1 binds to these mRNA targets directly and represses their translation. Additionally, we provide preliminary evidence that the Fxr1^(-/-) mice mimic a hypothyroid state of cardiac gene expression, with alterations in myosin heavy chain and troponin I isoforms. Our findings reveal the first mRNA targets of FXR1 in muscle and support translational repression as a novel mechanism for cardiac muscle development and function.

31

Richmond, Keith Neu 1950. "Critical oxygen tension measurements in striated muscle in vivo and in vitro." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/282258.

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The coupling of oxygen delivery to oxygen consumption is thought to occur as the result of an increase in the production of vasodilating substances which diffuse from the tissue and act on the smooth muscle of arterioles, resulting in an increase in regional blood flow (metabolic regulation). A majority of the hypotheses regarding the nature of metabolic regulation of blood flow focus on the role of cytochrome oxidase and oxidative phosphorylation. The oxygen tension (PO₂) at which the rate of cytochrome oxidase is one-half maximal (K(m)) has been determined in isolated mitochondria but has not been determined in vivo and some evidence suggests that it may be higher than in vitro. In these experiments we determine the PO₂ at which NADH fluorescence began to increase in vivo and in vitro in response to oxygen limitation (critical PO₂). These changes in fluorescence are assumed to reflect oxygen limitation of oxidative phosphorylation and can be compared to the cytochrome oxidase K(m) values. This assumption was tested using imaging techniques on single striated myocytes to determine whether the change in NADH fluorescence that occurs with oxygen removal was associated with mitochondrial dense regions. Our findings support the use of NADH fluorescence to monitor oxidative phosphorylation. Using this technique the critical PO₂ was measured at tissue sites in post-capillary venular regions and in 20 micron diameter post-capillary venules. The critical PO₂ in the tissue was 2.4 mmHg and was higher in the venule (7.7 mmHg), consistent with predicted diffusion gradients for oxygen from vessel to tissue. The difference between the extracellular tissue PO₂ and the of Km cytochrome oxidase for oxygen (.05-0.05 mmHg) is consistent with theorized gradients existing between cell membrane and mitochondria and does not necessarily indicate a higher critical PO₂ in vivo. Using techniques similar to those used in vivo we measured the critical PO₂ from single isolated striated cells and determined it was significantly different from the critical PO₂ measured in vivo. This difference is likely due to the differences between in vivo and in vitro measurement conditions rather than real differences in the critical PO₂.

32

Burnett, Colin Michael-Lee. "Striated muscle action potential assessment as an indicator of cellular energetic state." Thesis, University of Iowa, 2012. https://ir.uiowa.edu/etd/2830.

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Action potentials of striated muscle are created through movement of ions through membrane ion channels. ATP-sensitive potassium (KATP) channels are the only known channels that are gated by the intracellular energetic level ([ATP]/[ADP] ratio). KATP channels are both effectors and indicators of cellular metabolism as part of a negative feedback system. Decreased intracellular energetic level alters the gating of KATP channels, which is reflected in alterations of the action potential morphology. These changes protect the cell from exhaustion or injury by altering energy-consuming processes that are driven by membrane potential. Assessing the effects of KATP channel activation on resting membrane potential and action potential morphology, and the relationship to cellular stress is important to the understanding of normal cellular function. To better understand how muscle cells adapt to energetic stress, the monophasic action potential (MAP) electrode and floating microelectrode were used to record action potentials in intact hearts and skeletal muscles, respectively. Intact organs provide a more physiological environment for the study of energetics and membrane electrical phenomena. Utilizing these techniques, a stress on the intracellular energetic state resulted in greater and faster shortening of the duration of cardiac action potentials, and hyperpolarization of the membrane of skeletal muscle in a KATP channel dependent manner. Motion artifacts are a limitation to studying transmembrane action potentials, but the MAP and floating microelectrode techniques uniquely allow for reading of action potential morphology uncoupled from motion artifacts. The use of the floating microelectrode in skeletal muscles is a novel approach that provides previously unavailable data on skeletal muscle membrane potentials in situ.

33

Nabi, Md Ashikun. "Multiple Functions Of The Striated Rootlet Proteins Of The Paramecium Basal Body." ScholarWorks @ UVM, 2018. https://scholarworks.uvm.edu/graddis/951.

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Paramecium ciliary basal bodies align in straight rows from posterior to anterior. Each basal body is connected to three rootlets ((Post Ciliary Rootlet (PCR), Transverse Rootlet (TR) and Striated Rootlet (SR)). The SR, the longest, projects from the basal body toward the anterior past several more anterior basal bodies. The depletion of Meckelin (MKS3) misaligns SRs, disorganizes basal body rows and makes the SRs appear ragged and serpentine. In this study we clarify the composition of the Paramecium ciliary basal body’s SR and demonstrate that the SR plays a critical role in creating the orderly array of basal bodies in rows that run from pole to pole of the cell, likely through the interactions with centrins and other cytoskeletal elements underlying the cell surface. Here in this study we first report the reciprocal relationship between the SR and centrin related infraciliary lattice (ICL) protein that can dictate the cell surface morphology. The SR of Chlamydomonas is the best studied. Using the single SR Chlamydomonas gene SF-assemblin to search in Paramecium DB, we found thirty Paramecium genes in thirteen Paralog Groups. Proteins from 13 paralog groups were confirmed to be in the SR structure using immunofluorescence. LC-MS/MS analyses of density fractions from SRs isolation show all thirty SR members are within the same density fraction. We further categorized all 30 SR genes in five Structural Groups based on their ability to form coiled coil domain and evaluate the function of all five Structural Group using RNA interference (RNAi). Silencing the transcripts of the any of the Structural Group showed misaligned basal body rows and the disordered organization of the SRs with abnormal appearance of SRs all over the cell surface. Silencing of Paralog Group showed normal phenotype except for the two Paralog Group (Paralog Group 1 or Paralog Group 7) which themselves constitute Structural Group individually. Isolated SRs from the control or Paralog Group depleted cells show a characteristic striation pattern that includes characteristic major and minor striations. Isolated SRs from any of the Structural Group depleted cells demonstrate abnormal shapes and striation periodicity. There is a correlation between the SR Structural Group RNAi surface misalignment phenotype and the isolated SR Structural Group RNAi phenotype for shape and periodicity of the SR. Strikingly our study of SR clearly demonstrates the role of SRs in shaping the other cytoskeleton structures of the cell cortex e.g., ICL, epiplasm territory and cortical unit territory. In another follow up study of MKS3 (Picariello et al., 2014), we depleted the transcripts of MKS5 gene in Paramecium tetraurelia. Depletion of MKS5 transcripts in Paramecium causes cilia loss all over the cell surface. Unlike MKS3 depletion, MKS5 depletion does not affect the straight basal body rows and the ordered organization of SRs. Moreover, data presented in this study clearly demonstrates depletion of MKS5 transcripts somehow affect the localization of another transition zone protein, B9D2. It appears when lacking any of the SR Structural Group, the rest fail to interact properly with each other to maintain the SRs structure and directionality toward the anterior. As a result, abnormal SRs appear to lose the interaction with other cytoskeleton structures such as ICL network complex, which eventually results in misaligned basal body rows and altered swimming behavior. From the data presented in this study it is reasonable to postulate ICL1e subfamily and SRs are in a reciprocal relationship to maintain the straight basal body rows and the highly ordered organization of the SRs all over the cell surface.

34

Cheng, Bo. "Investigation of the control of major enzymes involved in adenosine metabolism in rat skeletal muscle /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20228399.

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35

Tonino, Paola, Balazs Kiss, Josh Strom, Mei Methawasin, John E. Smith, Justin Kolb, Siegfried Labeit, and Henk Granzier. "The giant protein titin regulates the length of the striated muscle thick filament." NATURE PUBLISHING GROUP, 2017. http://hdl.handle.net/10150/626066.

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The contractile machinery of heart and skeletal muscles has as an essential component the thick filament, comprised of the molecular motor myosin. The thick filament is of a precisely controlled length, defining thereby the force level that muscles generate and how this force varies with muscle length. It has been speculated that the mechanism by which thick filament length is controlled involves the giant protein titin, but no conclusive support for this hypothesis exists. Here we show that in a mouse model in which we deleted two of titin's C-zone super-repeats, thick filament length is reduced in cardiac and skeletal muscles. In addition, functional studies reveal reduced force generation and a dilated cardiomyopathy (DCM) phenotype. Thus, regulation of thick filament length depends on titin and is critical for maintaining muscle health.

36

Brenner, Tracy Lynn. "The physiology of crayfish intestinal striated muscle, histology, histochemistry, and excitation-contraction coupling." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ47992.pdf.

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37

Martin, Rex E. (Rex Edward). "Neuroregulation and Myosin Light Chain Phosphorylation in Ascaris Suum Obliquely Striated Skeletal Muscle." Thesis, North Texas State University, 1985. https://digital.library.unt.edu/ark:/67531/metadc504635/.

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Extraction and quantitation of myosin light chain two coupled with myograph recordings from Ascaris muscle perfused with calmodulin inhibitors and neurotransmitters in conjunction with their respective agonists and antagonists have been used to establish the regulation of contraction in this muscle. Densitometric tracings of isolectric focusing gels separating the regulatory light chain were used to quantitate phosphorylation in resting, contracted and flaccid muscle. These studies indicated that inhibitory neurostimulation is mediated by a true GABA receptor. Myosin-mediated contraction is responsible for maintaining the level of tension observed in resting actin-mediated muscle. Actin-mediated contraction is responsible for the rapid rise in tension following excitatory stimuli. Both systems function simultaneously and are independant.

38

Cheng, Bo, and 程菠. "Investigation of the control of major enzymes involved in adenosine metabolism in rat skeletal muscle." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31238269.

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39

Janes, Daniel Peter. "Structural and functional approaches to myosin linked regulation using expressed protein fragments." Thesis, Royal Veterinary College (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249481.

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40

Le, Gengyun. "Investigation of the enzymes involved in adenosine metabolism in vascular endothelial cells from rat skeletal muscle." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42182165.

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41

Ranasinghesagara, Janaka C. Yao Gang. "Optical reflectance in fibrous tissues and skeletal muscles." Diss., Columbia, Mo. : University of Missouri--Columbia, 2008. http://hdl.handle.net/10355/6629.

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Title from PDF of title page (University of Missouri--Columbia, viewed on March 8, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: Dr. Gang Yao. Vita. Includes bibliographical references.

42

Agarkova, Irina. "Functional diversity of contractile isoproteins : expression of actin and myomesin isoforms in striated muscle /." [S.l.] : [s.n.], 2000. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=13769.

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43

Connor, Michael K. "The regulation of gene expression in striated muscle during conditions of altered contractile activity." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0017/NQ56221.pdf.

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44

Smith, Kimberley Hazel. "Fast Fourier transform and dynamic imaging of caveolar complex arrays in active striated muscle." Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/8767.

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Appendix 2: Movie Clips is supplied as a Zip Archive and will need to be unzipped before viewing. The mechanism of force transfer from contracting sarcomeres to the membrane and endomysium of striated muscle fibres is unclear. The caveolar complex array in striated muscle membranes is a local concentration of cholesterol, sphingomyelin, signalling molecules and the protein caveolin-3. Immunofluorescence microscopy of caveolin-3 in the membrane reveals a regular pattern of fluorescent nodes arranged in longitudinal and transverse rows. The primary aim of this study was to analyse this pattern and how caveolin-3 behaves during contraction. Dynamic imaging and Fast Fourier Transforms (FFTs) were used to study force transmission across the fibre membrane. This pattern was studied in frozen sections of both shortened and rest-length striated muscle fibres. Direct and FFT measurements of spacings between these nodes demonstrated significant reductions in longitudinal measurements in shortened muscle when compared to rest-length muscle. Caveolin-3 nodes lay in register with underlying actin bands in both muscle states, and co-localised with dystrophin. Caveolin-3 was not detectable in C2C12 myoblasts. During differentiation expression became detectable at 2 days. Caveolin-3 was present during myoblast fusion, before forming the regular pattern on the membrane from days 4-5. Fibres became contractile after 5-6 days of development. By 12 days, muscle fibres are 1-2 mm long, multinucleated myotubes with evidence of the caveolin-3 immunofluorescence pattern seen in mature fibres. Knockdown of caveolin-3 expression greatly reduced the number of differentiated myotubes at 12 days. This pattern was not demonstrated in contracting myotubes, possibly owing to lack of permeability to the antibody. The results are consistent with the hypothesis that the force of contraction is transferred across the whole membrane rather than at fibre distal ends.

45

Eulitz, Stefan [Verfasser]. "Functional Analysis of the Xin-Repeat Protein Family in Cross-striated Muscle / Stefan Eulitz." Bonn : Universitäts- und Landesbibliothek Bonn, 2011. http://d-nb.info/1044857749/34.

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46

Kuo, Lih. "EFFECTS OF HEMATOCRIT VARIATIONS ON MICROCIRCULATORY HEMODYNAMICS AND OXYGEN TRANSPORT IN HAMSTER STRIATED MUSCLE." VCU Scholars Compass, 1987. https://scholarscompass.vcu.edu/etd/5131.

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Experiments were performed to investigate the influence of isovolemic hemodilution and hemoconcentration on microcirculatory hemodynamics and oxygen transport in the hamster cheek pouch retractor muscle. Measurements of red blood cell velocity, microvessel hematocrit, vessel diameter, segment length (L), hemoglobin oxygen saturation (SO2) and longitudinal SO2 gradient (ΔSO2/L) were made in four arteriolar branching orders before and after isovolemic exchange with plasma (hemodilution) or packed red blood cells (hemoconcentration). In the study of hemodilution, systemic hematocrit was reduced from 52 to 33% in 23 hamsters. This degree of hemodilution resulted in an average decrease in microcirculatory hematocrit from 42 to 28%, and average increases in red blood cell velocity, computed blood flow and systemic arterial oxygen tension (PO2) of 50%, 30% and 10%, respectively. In addition, ΔSO2/L was significantly smaller in second, third and fourth order arterioles compared with control values. It was estimated that about 16% of the oxygen that diffused across the arteriolar network was consumed by the surrounding tissue; the remaining oxygen was presumably transferred by diffusion to nearby venules and capillaries. Following hemodilution, the proportion of the diffusional loss that was consumed by the periarteriolar tissue increased to about 27%. Convective oxygen flow remained at its control level in the first order arterioles, and progressively increased above control with increasing branching order. The increased oxygen delivery to the capillary network following limited hemodilution can be attributed to a compensatory increase in blood flow, an increase in systemic arterial blood oxygenation, and a decrease in precapillary oxygen loss. In the study of hemoconcentration, systemic hematocrit was increased from 50% to 65% in 17 hamsters. Microcirculatory hematocrit increased from 40% to 50%, while the average red blood cell velocity and computed blood flow decreased approximately 40% and 30%, respectively. ΔSO2/L significantly increased in the four arteriolar branching orders compared with control values. It was estimated that about 10% of the oxygen that diffused across the arteriolar network was consumed by the surrounding tissue; the remaining 90% was presumably transferred by diffusion to nearby venules and capillaries. Convective oxygen flow again remained at its control level in the first order arterioles and progressively decreased below control in the more distal branching orders. Our analysis of arteriolar oxygen diffusion indicated that tissue oxygenation was unchanged following hemoconcentration, a result that can be attributed to a combined effect of decreased red blood cell velocity, increased precapillary oxygen loss, relatively unchanged diffusional shunting and arteriolar vasodilation. It appears that oxygen diffusion from arteriolar networks may play an important role in the regulation of tissue oxygenation during alterations of systemic hematocrit.

47

Ward, R. J. "Structural studies of the thick filament positions in the A-band of vertebrate striated muscle." Thesis, Open University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377345.

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48

Pieples, Kathy. "THE FUNCTIONAL SIGNIFICANCE OF THE STRIATED ISOFORM OF TROPOMYOSIN 3 IN NORMAL AND PATHOLOGICAL STATES." University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin997992638.

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49

Hudson, Liam. "Ultrastructure of the A-band unit cell in relaxed muscle." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310340.

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50

Sakkas, Georgios K. "End-stage renal failure and the composition of striated muscle pre- and post-exercise intervention strategy." Thesis, Manchester Metropolitan University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366178.

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