Relevant bibliographies by topics / Fibers Disarray

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Academic literature on the topic 'Fibers Disarray'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "Fibers Disarray"

1

Daliento, Luciano, Roldano Scognamiglio, Gaetano Thiene, Anita Hegerty, Siew Yen Ho, Francesca Caneve, and Robert H. Anderson. "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 (October 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, and disarrayed fibers. Comparable sections were obtained from six normal neonates to constitute a control group. Myocardial ischemia or infarction were frequent complications. Morphometric analysis demonstrated a significant difference between the control group and the patients with regard to the percentage of myocytes (longitudinal and transverse), the percentage of area occupied by myocardial disarray, and the presence of fibrosis. The highest values for the proportion of disarray were seen in those patients with small right ventricles. The percentage of myocytes varied, but the highest degree of disarray always correlated with the lowest percentage of myocytes. The highest percentage value of left ventricular disarray was associated with the lowest ratio of left ventricular mass to end diastolic volume (inadequate hypertrophy). The lowest indices of contractility and left ventricular pump function were associated with myocytes less than 55% of normal. A linear correlation was found between the percentage area of fibrosis and the ratio of systolic pressure to end systolic volume in the left ventricle, arid between fibrosis and ejection fraction. Values for fibrosis exceeding 15% were associated with decreased functional indices. Disarray, therefore, seems to express a primary inability of myocardium to respond to anomalous overload with adequate hypertrophy and/or hyperplasia.
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Kirschner, Sebastian E., Edgar Becker, Massimo Antognozzi, Hans-Peter Kubis, Antonio Francino, Francisco Navarro-López, Nana Bit-Avragim, et al. "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, no. 3 (March 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 from HCM patients of three families with selected myosin mutations. Fibers with the Arg723Gly and Arg719Trp mutations showed a decrease in mean pCa50, whereas those with the Ile736Thr mutation showed slightly increased mean pCa50 with higher active forces at low calcium concentrations and residual active force even under relaxing conditions. In addition, there was a marked variability in pCa50 between individual fibers carrying the same mutation ranging from an almost normal response to highly significant differences that were not observed in controls. While changes in mean pCa50 may suggest specific pharmacological treatment (e.g., calcium antagonists), the observed large functional variability among individual muscle cells might negate such selective treatment. More importantly, the variability in pCa50 from fiber to fiber is likely to cause imbalances in force generation and be the primary cause for contractile dysfunction and development of disarray in the myocardium.
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Pierantozzi, Enrico, Péter Szentesi, Cecilia Paolini, Beatrix Dienes, János Fodor, Tamás Oláh, Barbara Colombini, 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 (January 24, 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 the time to peak (TTP) and half relaxation time (HRT) were prolonged. Differences in force-frequency and force-velocity relationships and an enhanced fatigability are observed in an Obscn KO diaphragm with respect to WT controls. Voltage clamp experiments show that a sarcoplasmic reticulum’s Ca2+ release and SERCA reuptake rates were decreased in muscle fibers from Obscn KO mice, suggesting that an impairment in intracellular Ca2+ dynamics could explain the observed differences in the TTP and HRT in the diaphragm. In partial contrast with previous observations, Obscn KO mice show a normal exercise tolerance, but fiber damage, the altered sarcomere ultrastructure and M-band disarray are still observed after intense exercise.
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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 (January 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 ischemic tissue and rotated 90°. The slit altered systolic deformation in the infarcted tissue, changing circumferential strain from expansion to compression and increasing radial strain and shears and the variability of collagen fiber angles but not the mean angle. In the plug pigs, when deformation, matrix orientation, and continuity are altered in the infarct area, the result is complete disarray in the organization of collagen within the infarct scar.
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5

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 (August 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 branches. Eggs were scanty in the tissue sections, and matrix degradation probably represented involuting changes related to the progressive diminution of parasite-related aggression, which occurs spontaneously with age or after cure by chemotherapy. The changes indicative of matrix degradation now described are probably the basic morphological counterpart of periportal fibrosis involution currently being documented by ultrasonography in hepatosplenic patients submitted to curative chemotherapy.
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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 (August 1, 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 disarrayed septal myocardium was modeled by randomly distributed three-dimensional regions of altered material properties based on measured statistical distributions of muscle fiber angular dispersion. Material properties in disarrayed regions were modeled by decreased systolic anisotropy derived from increased fiber angle dispersion and decreased systolic tension development associated with reduced sarcomere lengths. Compared with measurements in ras transgenic mice, the model showed similar heterogeneity of septal systolic strain with the largest reductions in principal shortening and torsional shear in regions of greatest disarray. Average systolic principal shortening on the right ventricular septal surface of the model was −0.114 for normal regions and −0.065 for disarrayed regions; for torsional shear, these values were 0.047 and 0.019, respectively. These model results suggest that regional dysfunction in ras transgenic mice may be explained in part by the observed structural defects, including myofiber dispersion and reduced sarcomere length, which contributed about equally to predicted dysfunction in the disarrayed myocardium.
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Ritter, Paul, Stefanie Nübler, Andreas Buttgereit, Lucas R. Smith, Alexander Mühlberg, Julian Bauer, Mena Michael, 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 (September 16, 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- and intracellular architecture of whole muscle and single fibers from extensor digitorum longus (EDL) and diaphragm. Despite increased collagen contents in both muscles, passive stiffness in mdx Cmah−/− diaphragm was similar to wt mice (EDL muscles were twice as stiff). Isometric twitch and tetanic stresses were 50% reduced in mdx Cmah−/− diaphragm (15% in EDL). Myofibrillar architecture was severely compromised in mdx Cmah−/− single fibers of both muscle types, but more pronounced in diaphragm. Our results show that the mdx Cmah−/− genotype reproduces DMD-like fibrosis but is not associated with changes in passive visco-elastic muscle stiffness. Furthermore, detriments in active isometric force are compatible with the pronounced myofibrillar disarray of the dystrophic background.
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Hara, Hironori, Sonoko Maemura, Takayuki Fujiwara, Norifumi Takeda, Satoshi Ishii, Hiroki Yagi, Takaaki Suzuki, et al. "Inhibition of transforming growth factor-β signaling in myeloid cells ameliorates aortic aneurysmal formation in Marfan syndrome." PLOS ONE 15, no. 11 (November 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 infiltration and TGF-β signaling in the aorta. Aneurysmal formation with fragmentation and disarray of medial elastic fibers observed in MFS mice was significantly ameliorated in Fbn1C1039G/+;Tgfbr2MyeKO mice. In the aorta of Fbn1C1039G/+;Tgfbr2MyeKO mice, both canonical and noncanonical TGF-β signals were attenuated and the number of infiltrated F4/80-positive macrophages was significantly reduced. In vitro, TGF-β enhanced the migration capacity of RAW264.7 macrophages. These findings suggest that TGF-β signaling in myeloid cells promotes aortic aneurysmal formation and its inhibition might be a novel therapeutic target in MFS.
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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 (September 4, 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 precisely overlapped with dystrophin. However, costameric actin was absent from all sarcolemma isolated from dystrophin-deficient mdx mouse muscle even though it was localized to costameres in situ. Vinculin, α-actinin, β-dystroglycan and utrophin were all retained on mdx sarcolemma, indicating that the loss of costameric actin was not due to generalized membrane instability. Our data demonstrate that the dystrophin complex forms a mechanically strong link between the sarcolemma and the costameric cytoskeleton through interaction with γ-actin filaments. Destabilization of costameric actin filaments may also be an important precursor to the costamere disarray observed in dystrophin-deficient muscle. Finally, these methods will be broadly useful in assessing the mechanical integrity of the membrane cytoskeleton in dystrophic animal models lacking other costameric proteins.
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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 (July 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. In group I an initial loss of endothelial and smooth muscle cells along with elastin breakdown was followed by an impaired endothelial regeneration and significant graft wall thickening. The elastic tissue was replaced by collagen type I and chondroitin sulfate accumulations, which included a disarray of α-smooth muscle actin positive cells. The endothelium was preserved in group II. After 3 weeks the circumferential elastin layers were densified, distended and separated from the endothelium by a neointimal growth of irregular thickness. Biodegradable perivenous conduit minimized endothelial injury and allowed the partial preservation of elastin fibers and smooth muscle cells in the arteriovenous graft. It did not however, prevent myofibroblastic cell proliferation and triggered a macrophagic reaction.
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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 disfunction in entire organs is challenging, due to the inefficacy of standard imaging methods in performing high-resolution three-dimensional reconstructions in massive tissues. In this work, we developed a new full-optical correlative approach to quantify and integrate the electrical dysfunctions with three-dimensional structural reconstructions of entire hearts, both in controls and in a mouse model of ACM. We combined optical mapping of the action potential propagation (APP) with advances in tissue clearing and light-sheet microscopy techniques. First, we employed an optical platform to map and analyze the APP in Langendorff-perfused hearts. Then, we optimized the SHIELD procedure for the clearing of cardiac tissue, thus converting the previously electrically characterized samples into well-preserved and fully-transparent specimens. A high-throughput light-sheet microscope has been developed allowing the reconstruction of the whole mouse heart with a micrometric resolution allowing fine quantification of myocytes alignment and fibrosis deposition across the organ. Finally, we developed a software pipeline that employs high-resolution 3D images to analyze and co-register APP maps with the 3D anatomy, contractile fibers disarray, and fibrosis deposition on each heart. We found that although fiber disarray is not involved in this remodeling process, the accumulation of fibrotic patches found in the ACM mouse model can deform the propagating wavefront potentially facilitating the formation of reentry circuits. We believe that this promising methodological framework will allow clarifying the involvement of fine structural alterations in the electrical dysfunctions, thus enabling a unified investigation of the structural causes that lead to electrical and mechanical alterations after the tissue remodeling.
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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, 574–88. Oxford, UK: 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, 669–80. 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 involve the right ventricle, and an atrial myopathy may be progressive (left atrial enlargement and increased risks of atrial fibrillation). Right ventricle and left atrium involvement may be secondary to the left ventricular disease and/or a primary consequence of the basic molecular defect. The LVH represents hypertrophy and hyperplasia of several cell types, including cardiac myocytes, fibroblasts, and smooth muscle cells, along with excessive collagen and matrix deposition, and abnormalities of the microvasculature. The normal parallel arrangement of myocytes is often disturbed (fibre disarray).
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Knight, Charles, and Saidi A. Mohiddin. "Alcohol septal ablation for obstructive hypertrophic cardiomyopathy." In Oxford Textbook of Interventional Cardiology, 683–98. 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. Hypertrophy may involve the right ventricle (RV), and an atrial myopathy may be progressive (left atrial enlargement [LA) and increased risks of atrial fibrillation [AF]). RV and LA involvement may be secondary to the LV disease, and/or a primary consequence of the basic molecular defect. The LVH represents hypertrophy and hyperplasia of several cell types, including cardiac myocytes, fibroblasts, and smooth muscle cells, along with excessive collagen and matrix deposition, and abnormalities of the microvasculature. The normal parallel arrangement of myocytes is often disturbed (fibre disarray). Clinical practice addresses three needs: 1) assessing and treating the symptomatic patient; 2) assessing and addressing prognostic risks; and 3) genetic counselling, family screening, and mutation detection (genetic testing). Symptoms due to HCM will often have a striking variation in severity when patients may describe good and bad days, exacerbation of symptoms following large meals and an intolerance of dehydration or a hot climate. Chest pain, with a quality similar to angina pectoris but often developing at rest, dyspnoea, palpitations, dizziness, pre/syncope, and fatigue are the common complaints. Although the relief of LV outflow obstruction (LVOTO) by alcohol septal ablation (ASA) for the management of symptomatic HCM is the focus of this chapter, we will first describe some of the more important features of HCM in order that this procedure can be placed in the context of a complex cardiac condition.
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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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