Relevant bibliographies by topics / Fibers Disarray

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

Academic literature on the topic 'Fibers Disarray'

Author: Grafiati
Published: 14 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Fibers Disarray"

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Daliento, Luciano, Roldano Scognamiglio, Gaetano Thiene, et al. "Morphologic and functional analysis of myocardial status in pulmonary atresia with intact ventricular septum—an angiographic, histologic and morphometric study." Cardiology in the Young 2, no. 4 (1992): 361–66. http://dx.doi.org/10.1017/s1047951100007952.

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SummaryWe studied 11 patients with pulmonary atresia and intact ventricular septum who died at ages ranging from one day to three years. All but two neonates died after surgery. Pre-surgical catheterization with left and right cineventriculography was performed in nine patients, and quantitative parameters were calculated. By histologic examination of transverse transmural sections, the incidence and extent of myocardial ischemia or infarction were determined, as well as the percentage area per field occupied by vessels, myocytes orientated longitudinally or transversely, interstitial space, a
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Kirschner, Sebastian E., Edgar Becker, Massimo Antognozzi та ін. "Hypertrophic cardiomyopathy-related β-myosin mutations cause highly variable calcium sensitivity with functional imbalances among individual muscle cells". American Journal of Physiology-Heart and Circulatory Physiology 288, № 3 (2005): H1242—H1251. http://dx.doi.org/10.1152/ajpheart.00686.2004.

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Disease-causing mutations in cardiac myosin heavy chain (β-MHC) are identified in about one-third of families with hypertrophic cardiomyopathy (HCM). The effect of myosin mutations on calcium sensitivity of the myofilaments, however, is largely unknown. Because normal and mutant cardiac MHC are also expressed in slow-twitch skeletal muscle, which is more easily accessible and less subject to the adaptive responses seen in myocardium, we compared the calcium sensitivity (pCa50) and the steepness of force-pCa relations (cooperativity) of single soleus muscle fibers from healthy individuals and f
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Pierantozzi, Enrico, Péter Szentesi, Cecilia Paolini, et al. "Impaired Intracellular Ca2+ Dynamics, M-Band and Sarcomere Fragility in Skeletal Muscles of Obscurin KO Mice." International Journal of Molecular Sciences 23, no. 3 (2022): 1319. http://dx.doi.org/10.3390/ijms23031319.

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Obscurin is a giant sarcomeric protein expressed in striated muscles known to establish several interactions with other proteins of the sarcomere, but also with proteins of the sarcoplasmic reticulum and costameres. Here, we report experiments aiming to better understand the contribution of obscurin to skeletal muscle fibers, starting with a detailed characterization of the diaphragm muscle function, which we previously reported to be the most affected muscle in obscurin (Obscn) KO mice. Twitch and tetanus tension were not significantly different in the diaphragm of WT and Obscn KO mice, while
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Andrade, Zilton A., and Ediriomar Peixoto. "Pathology of periportal fibrosis involution in human schistosomiasis." Revista do Instituto de Medicina Tropical de São Paulo 34, no. 4 (1992): 263–72. http://dx.doi.org/10.1590/s0036-46651992000400001.

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Optical and electron microscopical evidences of focal matrix degradation were frequently seen in liver sections of periportal fibrosis caused by schistosomiasis mansoni in man. The material came from 14 wedge hepatic biopsies taken from patients with chronic advanced hepatosplenic disease and undergoing operations for the relief of portal hypertension. Besides the presence of focal areas of rarefaction, fragmentation and dispersion of collagen fibers, the enlarged portal spaces also showed hyperplasia of elastic tissue and disarray of smooth muscle fibers following destruction of portal vein b
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Zimmerman, Scott D., William J. Karlon, Jeffrey W. Holmes, Jeffrey H. Omens, and James W. Covell. "Structural and mechanical factors influencing infarct scar collagen organization." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 1 (2000): H194—H200. http://dx.doi.org/10.1152/ajpheart.2000.278.1.h194.

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Although large collagen fibers in myocardial infarct scar are highly organized, little is known about mechanisms controlling this organization. The preexisting extracellular matrix may act as a scaffold along which fibroblasts migrate. Conversely, deformation within the ischemic area could guide fibroblasts so new collagen is oriented to counteract the stretch. To investigate these potential mechanisms, we infarcted three groups of pigs. Group 1 served as infarct controls. Group 2 had the endocardium slit longitudinally to alter local systolic deformation. Group 3had a plug sectioned from isch
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Ritter, Paul, Stefanie Nübler, Andreas Buttgereit, et al. "Myofibrillar Lattice Remodeling Is a Structural Cytoskeletal Predictor of Diaphragm Muscle Weakness in a Fibrotic mdx (mdx Cmah−/−) Model." International Journal of Molecular Sciences 23, no. 18 (2022): 10841. http://dx.doi.org/10.3390/ijms231810841.

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Duchenne muscular dystrophy (DMD) is a degenerative genetic myopathy characterized by complete absence of dystrophin. Although the mdx mouse lacks dystrophin, its phenotype is milder compared to DMD patients. The incorporation of a null mutation in the Cmah gene led to a more DMD-like phenotype (i.e., more fibrosis). Although fibrosis is thought to be the major determinant of ‘structural weakness’, intracellular remodeling of myofibrillar geometry was shown to be a major cellular determinant thereof. To dissect the respective contribution to muscle weakness, we assessed biomechanics and extra-
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Usyk, T. P., J. H. Omens, and A. D. McCulloch. "Regional septal dysfunction in a three-dimensional computational model of focal myofiber disarray." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 2 (2001): H506—H514. http://dx.doi.org/10.1152/ajpheart.2001.281.2.h506.

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MLC2v/ ras transgenic mice display a phenotype characteristic of hypertrophic cardiomyopathy, with septal hypertrophy and focal myocyte disarray. Experimental measurements of septal wall mechanics in ras transgenic mice have previously shown that regions of myocyte disarray have reduced principal systolic shortening, torsional systolic shear, and sarcomere length. To investigate the mechanisms of this regional dysfunction, a three-dimensional prolate spheroidal finite-element model was used to simulate filling and ejection in the hypertrophied mouse left ventricle with septal disarray. Focally
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Hara, Hironori, Sonoko Maemura, Takayuki Fujiwara та ін. "Inhibition of transforming growth factor-β signaling in myeloid cells ameliorates aortic aneurysmal formation in Marfan syndrome". PLOS ONE 15, № 11 (2020): e0239908. http://dx.doi.org/10.1371/journal.pone.0239908.

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Increased transforming growth factor-β (TGF-β) signaling contributes to the pathophysiology of aortic aneurysm in Marfan syndrome (MFS). Recent reports indicate that a small but significant number of inflammatory cells are infiltrated into the aortic media and adventitia in MFS. However, little is known about the contribution of myeloid cells to aortic aneurysmal formation. In this study, we ablated the TGF-β type II receptor gene Tgfbr2 in myeloid cells of Fbn1C1039G/+ MFS mice (Fbn1C1039G/+;LysM-Cre/+;Tgfbr2fl/fl mice, hereinafter called Fbn1C1039G/+;Tgfbr2MyeKO) and evaluated macrophage inf
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Rybakova, Inna N., Jitandrakumar R. Patel, and James M. Ervasti. "The Dystrophin Complex Forms a Mechanically Strong Link between the Sarcolemma and Costameric Actin." Journal of Cell Biology 150, no. 5 (2000): 1209–14. http://dx.doi.org/10.1083/jcb.150.5.1209.

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The absence of dystrophin complex leads to disorganization of the force-transmitting costameric cytoskeleton and disruption of sarcolemmal membrane integrity in skeletal muscle. However, it has not been determined whether the dystrophin complex can form a mechanically strong bond with any costameric protein. We performed confocal immunofluorescence analysis of isolated sarcolemma that were mechanically peeled from skeletal fibers of mouse hindlimb muscle. A population of γ-actin filaments was stably associated with sarcolemma isolated from normal muscle and displayed a costameric pattern that
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Bambang, L. S., M. Moczar, L. Lecerf, and D. Loisance. "External Biodegradable Supporting Conduit Protects Endothelium in Vein Graft in Arterial Interposition." International Journal of Artificial Organs 20, no. 7 (1997): 397–406. http://dx.doi.org/10.1177/039139889702000708.

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The prevention of circumferential distension could reduce structural damage in arteriovenous grafts. We studied the effect of an external biodegradable supporting conduit on the endothelium and extracellular matrix in vein graft in a pig model. Cephalic vein control grafts (Group I) and jugular veins wrapped in a vicryl mesh tube (I.D. 4mm) (Group II) were implanted into autologous carotid arteries (n=14). The grafts were explanted after 1 and 24 hours and at 1 and 3 weeks and evaluated by ELISA for endothelial DNA synthesis and by immunohistoenzymic assays for cells and extracellular matrix.
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Dissertations / Theses on the topic "Fibers Disarray"

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Giardini, Francesco. "Morpho-functional investigation of cardiac remodeling in an arrhythmogenic mouse model by advanced optical methods." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1211015.

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Severe remodeling processes may occur in the heart due to both genetic and non-genetic diseases. Structural remodeling, such as collagen deposition (fibrosis) and cellular misalignment, can affect electrical conduction at different orders of magnitude and, eventually, lead to arrhythmias. In this scenario, arrhythmogenic cardiomyopathy (ACM) is an inherited heart disease that involves ventricular dysfunction, arrhythmias, and localized replacement of contractile fibers with fibrofatty scar tissue. Unfortunately, nowadays, redicting the impact of fine structural alterations on the electrical d
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Book chapters on the topic "Fibers Disarray"

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Giannakidis, Archontis, Damien Rohmer, Alexander I. Veress, and Grant T. Gullberg. "Diffusion Tensor Magnetic Resonance Imaging-Derived Myocardial Fiber Disarray in Hypertensive Left Ventricular Hypertrophy: Visualization, Quantification and the Effect on Mechanical Function." In Cardiac Mapping. Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481585.ch53.

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Knight, Charles, Saidi Mohiddin, and Constantinos O’Mahony. "Alcohol septal ablation for obstructive hypertrophic cardiomyopathy." In Oxford Textbook of Interventional Cardiology, edited by Simon Redwood, Nick Curzen, and Adrian Banning. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754152.003.0045.

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Hypertrophic cardiomyopathy (HCM) is a genetic disease occurring in up to 1 in 500 of the general population. HCM is often undiagnosed or misdiagnosed, and asymptomatic cases are often unrecognized. Asymmetric left ventricular hypertrophy (LVH) most often develops during the period of rapid body growth of adolescence, but it may be present in childhood or even before birth. Progressive LVH after age 20 is uncommon, but initial diagnosis even in old age is not. The hypertrophy predominantly involves the left ventricle, and is often more marked than in any other cardiac disease. Hypertrophy may
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Knight, Charles, and Saidi A. Mohiddin. "Alcohol septal ablation for obstructive hypertrophic cardiomyopathy." In Oxford Textbook of Interventional Cardiology. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199569083.003.041.

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Hypertrophic cardiomyopathy (HCM) is a genetic disease occurring in approximately one in 500–1000 of the general population. HCM is often undiagnosed or misdiagnosed, and asymptomatic cases are often unrecognized. Asymmetric left ventricular (LV) hypertrophy (LVH) most often develops during the period of rapid body growth of adolescence, but it may be present in childhood or, rarely, before birth. Progressive LVH after age 20 is uncommon, but initial diagnosis even in old age is not. The hypertrophy predominantly involves the LV, and is often more marked than in any other cardiac disease. Hype
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Conference papers on the topic "Fibers Disarray"

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Veress, A. I., A. Giannakidis, and G. T. Gullberg. "Mechanical Effects of Myofibril Disarray on Cardiac Function." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14696.

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Myocardial disarray is a fiber distribution that deviates away from the tightly organized, parallel alignment of myocardial fibers that characterizes the normal myocardium. This coherently-organized distribution of the myofibers results in the twisting contraction of the normal left ventricle (LV). With myofiber disarray, the fibers have random directionality, either locally or globally, within the LV.
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Journal articles
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