Thematische Bibliographien / Fibers Disarray / Zeitschriftenartikel
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Zeitschriftenartikel zum Thema „Fibers Disarray“

Autor: Grafiati
Veröffentlicht am 14. März 2023
Zuletzt aktualisiert am 31. Juli 2025

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1

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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Nascimento, Juliana Minardi, Gilberto Carlos Franchi, Alexandre Eduardo Nowill, Carla Beatriz Collares-Buzato, and Stephen Hyslop. "Cytoskeletal rearrangement and cell death induced by Bothrops alternatus snake venom in cultured Madin–Darby canine kidney cells." Biochemistry and Cell Biology 85, no. 5 (2007): 591–605. http://dx.doi.org/10.1139/o07-067.

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Bothrops snake venoms cause renal damage, with renal failure being the main cause of death in humans bitten by these snakes. In this work, we investigated the cytoskeletal rearrangement and cytotoxicity caused by Bothrops alternatus venom in cultured Madin–Darby canine kidney (MDCK) cells. Incubation with venom (10 and 100 µg/mL) significantly (p <0.05) decreased the cellular uptake of neutral red dye after 1 and 3 h. Venom (100 µg/mL) also markedly decreased the transepithelial electrical resistance (RT) across MDCK monolayers. Staining with rhodamine-conjugated phalloidin revealed disarra
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Protasi, Feliciano, Laura Pietrangelo, and Simona Boncompagni. "Improper Remodeling of Organelles Deputed to Ca2+ Handling and Aerobic ATP Production Underlies Muscle Dysfunction in Ageing." International Journal of Molecular Sciences 22, no. 12 (2021): 6195. http://dx.doi.org/10.3390/ijms22126195.

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Proper skeletal muscle function is controlled by intracellular Ca2+ concentration and by efficient production of energy (ATP), which, in turn, depend on: (a) the release and re-uptake of Ca2+ from sarcoplasmic-reticulum (SR) during excitation–contraction (EC) coupling, which controls the contraction and relaxation of sarcomeres; (b) the uptake of Ca2+ into the mitochondrial matrix, which stimulates aerobic ATP production; and finally (c) the entry of Ca2+ from the extracellular space via store-operated Ca2+ entry (SOCE), a mechanism that is important to limit/delay muscle fatigue. Abnormalitie
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Larregina, Adriana, Ana R. Hernändez, Olga Pis Diez, Graciela Quijano, and Ricardo Drut. "Biventricular Hypoplasia with Myocardial Fiber Hypertrophy and Disarray." Pediatric Pathology 10, no. 6 (1990): 993–99. http://dx.doi.org/10.3109/15513819009064733.

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Milei, J., R. Migliore, F. Guerrero, C. Pedroza, and R. Storino. "Muscle Fiber Disarray in Patients without Hypertrophic Cardiomyopathy." Cardiology 72, no. 3 (1985): 105–12. http://dx.doi.org/10.1159/000173850.

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Chen, Junjie, Sheng-Kwei Song, Wei Liu, et al. "Remodeling of cardiac fiber structure after infarction in rats quantified with diffusion tensor MRI." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 3 (2003): H946—H954. http://dx.doi.org/10.1152/ajpheart.00889.2002.

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Structural remodeling of myocardium after infarction plays a critical role in functional adaptation. Diffusion tensor magnetic resonance imaging (DTMRI) provides a means for rapid and nondestructive characterization of the three-dimensional fiber architecture of cardiac tissues. In this study, microscopic structural changes caused by MI were evaluated in Fischer 344 rats 4 wk after infarct surgery. DTMRI studies were performed on 15 excised, formalin-fixed rat hearts of both infarct (left anterior descending coronary artery occlusion, n = 8) and control (sham, n = 7) rats. Infarct myocardium e
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Tseng, Wen-Yih I., Jiangang Dou, Timothy G. Reese, and Van J. Wedeen. "Imaging myocardial fiber disarray and intramural strain hypokinesis in hypertrophic cardiomyopathy with MRI." Journal of Magnetic Resonance Imaging 23, no. 1 (2005): 1–8. http://dx.doi.org/10.1002/jmri.20473.

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Reed, Umbertina Conti, Maria Bernardete Dutra Resende, Lúcio Gobbo Ferreira, et al. "King-Denborough Syndrome: report of two Brazilian cases." Arquivos de Neuro-Psiquiatria 60, no. 3B (2002): 739–41. http://dx.doi.org/10.1590/s0004-282x2002000500011.

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We report on two boys aged 2 and 6 years-old respectively with dysmorphic face, ptosis, down-slanting palpebral fissures, hypertelorism, epicanthic folds, low-set ears, malar hypoplasia, micrognathia, high-arched palate, clinodactyly, palmar simian line, pectus excavatum, winging of the scapulae, lumbar lordosis and mild thoracic scoliosis who present congenital hypotonia, slightly delayed motor development, diffuse joint hyperextensibility and mild proximal weakness. The muscle biopsy revealed minimal but identifiable changes represented by size fiber variability, type I fiber predominance an
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Tezuka, Fumiaki, Ikuro Sato, Hiroki Mori, Masuko Nomura, and Waldemar Hort. "Quantitative Analysis of Fiber Disarray Developing in Papillary Muscles Unloaded after Mitral Valve Replacement." Pathology International 39, no. 12 (1989): 779–85. http://dx.doi.org/10.1111/j.1440-1827.1989.tb02430.x.

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Jain, Akshat, Jaiswal Vidyaagar, and Ravi Raghvan. "Sickle Cell Disease with Dermatomyositis - a Rare and Complex Comorbidity." Blood 138, Supplement 1 (2021): 4174. http://dx.doi.org/10.1182/blood-2021-148878.

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Abstract Introduction and Case Presentation - A 4 yrs old female with sickle cell disease (SCD) and intermittent asthma presented with polyarthralgia predominantly involving bilateral hip and knee joints and became non-ambulatory over a course of 2 months. She developed chronic facial swelling, and a pruritic erythematous rash involving face, extensor surface of the hand and the right knee with significant weight loss. Physical examination was significant for heliotropic rash on the eyelids, Also present were Gottron's papules and macules on both hands and right knee along with right leg tende
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Liu, Min, Yunfei You, Huaiyi Zhu, Yu Chen, Zhenying Hu, and Jingjing Duan. "N-Acetylcysteine Alleviates Impaired Muscular Function Resulting from Sphingosine Phosphate Lyase Functional Deficiency-Induced Sphingoid Base and Ceramide Accumulation in Caenorhabditis elegans." Nutrients 16, no. 11 (2024): 1623. http://dx.doi.org/10.3390/nu16111623.

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Sphingosine-1-phosphate lyase (SPL) resides at the endpoint of the sphingolipid metabolic pathway, catalyzing the irreversible breakdown of sphingosine-1-phosphate. Depletion of SPL precipitates compromised muscle morphology and function; nevertheless, the precise mechanistic underpinnings remain elusive. Here, we elucidate a model of SPL functional deficiency in Caenorhabditis elegans using spl-1 RNA interference. Within these SPL-deficient nematodes, we observed diminished motility and perturbed muscle fiber organization, correlated with the accumulation of sphingoid bases, their phosphoryla
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Wang, Y., K. Zhang, N. B. Wasala, D. Duan, and G. Yao. "Optical polarization tractography revealed significant fiber disarray in skeletal muscles of a mouse model for Duchenne muscular dystrophy." Biomedical Optics Express 6, no. 2 (2015): 347. http://dx.doi.org/10.1364/boe.6.000347.

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Raghunathan, Suchi, Pratik Tank, Shraddha Bhadada, and Bhoomika Patel. "Evaluation of Buspirone on Streptozotocin Induced Type 1 Diabetes and Its Associated Complications." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/948427.

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We have evaluated the effect of buspirone (1.5 mg/kg/day, p.o.) type 1 diabetes induced cardiovascular complications induced by streptozotocin (STZ, 45 mg/kg, i.v.) in Wistar rats. Various biochemical, cardiovascular, and hemodynamic parameters were measured at the end of 8 weeks of treatment. STZ produced significant hyperglycaemia, hypoinsulinemia, and dyslipidemia, which was prevented by buspirone treatment. STZ produced increase in serum creatinine, urea, lactate dehydrogenase, creatinine kinase, and C-reactive protein levels and treatment with buspirone produced reduction in these levels.
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Li, Chengcheng, Yang Liu, Handing Mao, Wenjun Yang, Shuyuan Liu, and Yi Shan. "Oncosis is the predominant type of cell death in rhabdomyolysis following exertional heat stroke." PLOS ONE 20, no. 3 (2025): e0308586. https://doi.org/10.1371/journal.pone.0308586.

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Background Rhabdomyolysis (RM), particularly heat exhaustion-associated rhabdomyolysis (ehsRM), is a significant clinical issue associated with high mortality and healthcare costs. However, the cellular death mechanisms remain incompletely understood. Oncosis, a form of passive cell death distinct from apoptosis, is characterized by cell swelling and triggered by ATP depletion. Additionally, porimin, a specific biomarker, can uniquely identify oncosis. This study aims to investigate the role and mechanisms of oncosis in both in vitro and in vivo models of ehsRM. Objective This study aims to in
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Warmke, J., M. Yamakawa, J. Molloy, S. Falkenthal, and D. Maughan. "Myosin light chain-2 mutation affects flight, wing beat frequency, and indirect flight muscle contraction kinetics in Drosophila." Journal of Cell Biology 119, no. 6 (1992): 1523–39. http://dx.doi.org/10.1083/jcb.119.6.1523.

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We have used a combination of classical genetic, molecular genetic, histological, biochemical, and biophysical techniques to identify and characterize a null mutation of the myosin light chain-2 (MLC-2) locus of Drosophila melanogaster. Mlc2E38 is a null mutation of the MLC-2 gene resulting from a nonsense mutation at the tenth codon position. Mlc2E38 confers dominant flightless behavior that is associated with reduced wing beat frequency. Mlc2E38 heterozygotes exhibit a 50% reduction of MLC-2 mRNA concentration in adult thoracic musculature, which results in a commensurate reduction of MLC-2
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TANAKA, MASARU, HISAYOSHI FUJIWARA, TOMOYA ONODERA, et al. "Pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis in normal hearts, hypertensive hearts and hearts with hypertrophic cardiomyopathy." Japanese Circulation Journal 51, no. 6 (1987): 624–30. http://dx.doi.org/10.1253/jcj.51.624.

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Zhang, Qinghai, Xiao He, Shihao Yao, et al. "Ablation of Mto1 in zebrafish exhibited hypertrophic cardiomyopathy manifested by mitochondrion RNA maturation deficiency." Nucleic Acids Research 49, no. 8 (2021): 4689–704. http://dx.doi.org/10.1093/nar/gkab228.

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Abstract Deficient maturations of mitochondrial transcripts are linked to clinical abnormalities but their pathophysiology remains elusive. Previous investigations showed that pathogenic variants in MTO1 for the biosynthesis of τm5U of tRNAGlu, tRNAGln, tRNALys, tRNATrp and tRNALeu(UUR) were associated with hypertrophic cardiomyopathy (HCM). Using mto1 knock-out(KO) zebrafish generated by CRISPR/Cas9 system, we demonstrated the pleiotropic effects of Mto1 deficiency on mitochondrial RNA maturations. The perturbed structure and stability of tRNAs caused by mto1 deletion were evidenced by confor
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Pugliese, Luca, Alessandra Luciano, and Marcello Chiocchi. "The Role of Cardiac Magnetic Resonance Imaging in the Management of Hypertrophic Cardiomyopathy." Journal of Cardiovascular Development and Disease 12, no. 5 (2025): 189. https://doi.org/10.3390/jcdd12050189.

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Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiomyopathy, caused by either sarcomere protein or other gene mutations. It is a complex and highly heterogeneous disorder, with phenotypes ranging from asymptomatic to severe disease, characterized by asymmetric left ventricular (LV) hypertrophy unexplained by loading conditions, which is also associated with myocardial fiber disarray, and preserved or increased ejection fraction without LV dilation. Comprehensive personal and family history, physical examination, and ECG testing raise suspicion of HCM, and echocardiogram represe
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Takayama, Yoshihisa, Yumi Okazaki, Tadashi Aruga, and Kashiko Kodate. "Hologram multiplexing with distorted wavefront and disarrayed polarization by use of a fiber bundle in rotary movement." Optics Communications 242, no. 4-6 (2004): 411–15. http://dx.doi.org/10.1016/j.optcom.2004.09.015.

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Russell, Noirin E., Peter Holloway, Stephen Quinn, Michael Foley, Peter Kelehan, and Fionnuala M. McAuliffe. "Cardiomyopathy and Cardiomegaly in Stillborn Infants of Diabetic Mothers." Pediatric and Developmental Pathology 11, no. 1 (2008): 10–14. http://dx.doi.org/10.2350/07-05-0277.1.

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To report the incidence of cardiomegaly in stillborn normally formed infants of mothers with diabetes mellitus. This is a retrospective study with institutional ethics approval. The presence of cardiomegaly was recorded in stillborn infants of diabetic mothers ( N = 27) and compared with that recorded in stillborn large-for–gestational age (LGA > 90th percentile, n = 18) and stillborn appropriately grown (10th to 90th percentiles, n = 107) nondiabetic infants. Blinded to the clinical details, the histology slides were reviewed to measure cardiac wall thickness and to record the presence or
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Pop Moldovan, Adina, Simona Dumitra, Cristina Popescu, et al. "Protective Effects of Hesperetin on Cardiomyocyte Integrity and Cytoskeletal Stability in a Murine Model of Epirubicin-Induced Cardiotoxicity: A Histopathological Study." Applied Sciences 14, no. 6 (2024): 2560. http://dx.doi.org/10.3390/app14062560.

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Anthracyclines, including epirubicin (Epi), are effective chemotherapeutics but are known for their cardiotoxic side effects, primarily inducing cardiomyocyte apoptosis. This study investigates the protective role of hesperetin (HSP) against cardiomyopathy triggered by Epi in a murine model. Male CD1 mice were divided into four groups, with the Epi group receiving a cumulative dose of 12 mg/kg intraperitoneally, reflecting a clinically relevant dosage. The co-treatment group received 100 mg/kg of HSP daily for 13 days. After the treatment period, mice were euthanized, and heart tissues were co
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Valberg, Stephanie J., Sudeep Perumbakkam, Erica C. McKenzie, and Carrie J. Finno. "Proteome and transcriptome profiling of equine myofibrillar myopathy identifies diminished peroxiredoxin 6 and altered cysteine metabolic pathways." Physiological Genomics 50, no. 12 (2018): 1036–50. http://dx.doi.org/10.1152/physiolgenomics.00044.2018.

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Equine myofibrillar myopathy (MFM) causes exertional muscle pain and is characterized by myofibrillar disarray and ectopic desmin aggregates of unknown origin. To investigate the pathophysiology of MFM, we compared resting and 3 h postexercise transcriptomes of gluteal muscle and the resting skeletal muscle proteome of MFM and control Arabian horses with RNA sequencing and isobaric tags for relative and absolute quantitation analyses. Three hours after exercise, 191 genes were identified as differentially expressed (DE) in MFM vs. control muscle with >1 log2 fold change (FC) in genes involv
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Benoist, David, Rachel Stones, Mark J. Drinkhill, et al. "Cardiac arrhythmia mechanisms in rats with heart failure induced by pulmonary hypertension." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 11 (2012): H2381—H2395. http://dx.doi.org/10.1152/ajpheart.01084.2011.

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Pulmonary hypertension provokes right heart failure and arrhythmias. Better understanding of the mechanisms underlying these arrhythmias is needed to facilitate new therapeutic approaches for the hypertensive, failing right ventricle (RV). The aim of our study was to identify the mechanisms generating arrhythmias in a model of RV failure induced by pulmonary hypertension. Rats were injected with monocrotaline to induce either RV hypertrophy or failure or with saline (control). ECGs were measured in conscious, unrestrained animals by telemetry. In isolated hearts, electrical activity was measur
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Ibrahim, D., and A. Gohara. "Unusual Death; Light Microscopy Solves The Mystery With An Archetypal Depiction Of An Unexpected Rare Cause." American Journal of Clinical Pathology 154, Supplement_1 (2020): S81. http://dx.doi.org/10.1093/ajcp/aqaa161.177.

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Abstract Casestudy: Hypertrophic cardiomyopathy is a heterogeneous disease with a number of phenotypes. We present the rarest phenotype, 1% of all cases, the midventricular obstructive type. It is characterized by hypertrophy in the mid portion of the left ventricle involving the papillary muscles, resulting in systolic intraluminal obstruction of the mid-ventricle. An unusual case of a 41-year-old male who died suddenly while hiking. He had no past medical history except for hyperlipidemia. He had no history of hypertension, with documented repeated normal blood pressures. No family history o
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Yuan, Ma, Zhang, and Jing. "Transforming growth factor-beta signaling pathway in Marfan’s syndrome: a preliminary histopathological study." Vasa 40, no. 5 (2011): 369–74. http://dx.doi.org/10.1024/0301-1526/a000133.

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Background: Marfan’s syndrome is an inherited disorder that affects the connective tissue. It has been proposed that mutations of FBN1 gene or of transforming growth factor (TGF)-beta type II receptor may be responsible for its pathogenesis. However, the role of TGF-beta signaling pathway in the development of Marfan’s syndrome has not been comprehensively investigated. Materials and methods: Surgical specimens of the aorta were obtained from two female Marfan patients, and the control aortic tissue was taken from an autopsy of a healthy individual. The aortic specimens were examined with hema
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Civitarese, Robert A., Ilana Talior-Volodarsky, Melissa Mitchell, et al. "Abstract 17939: Lack of the Alpha-11 Integrin in the Heart is Associated With Progressive Diastolic Dysfunction, Myofibrillar Disarray and Impaired Cardiomyocyte Growth." Circulation 130, suppl_2 (2014). http://dx.doi.org/10.1161/circ.130.suppl_2.17939.

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BACKGROUND: Integrins, transmembrane receptors, play crucial roles in diverse cellular and developmental processes due to critical interactions with the extracellular matrix (ECM). During fetal development and towards adulthood, heart growth and function is suggested to depend on forming and remodeling the ECM and its connection to the myocyte. Currently however, the role of integrins in cardiovascular development (CVD) is poorly defined. Thus, we hypothesized that the α11 integrin (α11), which is expressed by fibroblasts and binds preferentially to type I collagen fibers, plays a vital role i
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Green, Eric M., Robert M. Weiss, Abhay Divekar, et al. "Abstract 16: A Minipig Genetic Model of Hypertrophic Cardiomyopathy." Circulation Research 121, suppl_1 (2017). http://dx.doi.org/10.1161/res.121.suppl_1.16.

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Introduction: Hypertrophic cardiomyopathy (HCM) is a heritable disease of heart muscle associated with increased risk of heart failure and sudden death. Mutations in genes encoding sarcomere proteins are commonly associated with HCM. However, the mechanisms by which these mutations lead to molecular, cellular and organ-level pathophysiology are uncertain, partly because of the lack of model systems amenable to integrated translational studies. Methods: Using homologous recombination and somatic cell nuclear transfer, we generated Yucatan minipigs with a heterozygous knock-in of the R403Q mutat
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Wu, Yupeng, Yuzhu Zhang, Qirui Zheng, et al. "Myocardial dysfunction caused by MyBPC3 P459fs mutation in hypertrophic cardiomyopathy: evidence from multi-omics approaches and super-resolution imaging." Frontiers in Cardiovascular Medicine 12 (February 27, 2025). https://doi.org/10.3389/fcvm.2025.1529921.

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IntroductionMutations in the sarcomere protein, particularly in cardiac myosin binding protein C gene (MyBPC3), were the most frequent genetic cause of hypertrophic cardiomyopathy (HCM). The pathogenic MyBPC3 P459fs mutation has been reported in HCM patients. However, there was limited knowledge of the structure–function relationships and potential pathways in clinical HCM with MyBPC3 P459fs mutation.MethodsWe used multi-omics approaches and super-resolution imaging to explore the effects of MyBPC3 P459fs mutation on humans and cells. HCM patients carrying MyBPC3 P459fs mutation (MyBPC3-P459fs
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Chen, Peng, Bo Yu, Zongzhe Li, Yanghui Chen, Yang Sun та Dao Wen Wang. "COL5A1 Variants Cause Aortic Dissection by Activating TGF‐β‐Signaling Pathway". Journal of the American Heart Association 10, № 11 (2021). http://dx.doi.org/10.1161/jaha.120.019276.

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Background Aortic dissection (AD) is one of the most life‐threatening cardiovascular diseases that exhibit high genetic heterogeneity. However, it is unclear whether variants within the COL5A1 gene can cause AD. Therefore, we intend to determine whether COL5A1 is a causative gene of AD. Methods and Results We performed targeted sequencing in 702 patients with unrelated sporadic AD and 163 matched healthy controls using a predesigned panel with 152 vessel matrix‐related genes. As a result, we identified that 11 variants in COL5A1 caused AD in 11 out of the 702 patients with AD. Furthermore, Col
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Chen, Jiyuan, Callie Kwartler, Christina L. Papke та ін. "Abstract 458: Loss of Smooth Muscle α-actin in Mice Results in Thoracic Aortic Aneurysms via Increased Reactive Oxygen Species, Increased Nox4,and Increased Angiotensin II type 1 Receptor-Mediated Signaling". Arteriosclerosis, Thrombosis, and Vascular Biology 35, suppl_1 (2015). http://dx.doi.org/10.1161/atvb.35.suppl_1.458.

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Objective: ACTA2 mutations cause 10-14% of familial thoracic aortic aneurysms and dissections. Mice deficient in smooth muscle α-actin (Acta2-/-) develop root and ascending thoracic aortic enlargement associated with thickening of the aortic media and fragmentation and disarray of elastic fibers. We hypothesized that blocking AT1 activation would block the aortic pathology and prevent aortic enlargement in Acta2-/- mice. Methods and Results: Beginning at 4 weeks of age, Acta2-/- mice were treated with losartan or placebo (n≥10) for 6 months and echocardiograms were performed at baseline and ev
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Williams, Zoë J., Deborah Velez-Irizarry, Keri Gardner, and Stephanie J. Valberg. "Integrated proteomic and transcriptomic profiling identifies aberrant gene and protein expression in the sarcomere, mitochondrial complex I, and the extracellular matrix in Warmblood horses with myofibrillar myopathy." BMC Genomics 22, no. 1 (2021). http://dx.doi.org/10.1186/s12864-021-07758-0.

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Abstract Background Myofibrillar myopathy in humans causes protein aggregation, degeneration, and weakness of skeletal muscle. In horses, myofibrillar myopathy is a late-onset disease of unknown origin characterized by poor performance, atrophy, myofibrillar disarray, and desmin aggregation in skeletal muscle. This study evaluated molecular and ultrastructural signatures of myofibrillar myopathy in Warmblood horses through gluteal muscle tandem-mass-tag quantitative proteomics (5 affected, 4 control), mRNA-sequencing (8 affected, 8 control), amalgamated gene ontology analyses, and immunofluore
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Remex, Naznin Sultana, Chowdhury S. Abdullah, Richa Aishwarya, et al. "Deletion of Sigmar1 leads to increased arterial stiffness and altered mitochondrial respiration resulting in vascular dysfunction." Frontiers in Physiology 15 (April 29, 2024). http://dx.doi.org/10.3389/fphys.2024.1386296.

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Sigmar1 is a ubiquitously expressed, multifunctional protein known for its cardioprotective roles in cardiovascular diseases. While accumulating evidence indicate a critical role of Sigmar1 in cardiac biology, its physiological function in the vasculature remains unknown. In this study, we characterized the expression of Sigmar1 in the vascular wall and assessed its physiological function in the vascular system using global Sigmar1 knockout (Sigmar1−/−) mice. We determined the expression of Sigmar1 in the vascular tissue using immunostaining and biochemical experiments in both human and mouse
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Phan, Noel M., Arick Park, Ting Zhou, et al. "Abstract 183: Collagen Type V (Col V) Contributes to the Development of Aortic Dissections and Aneurysms." Arteriosclerosis, Thrombosis, and Vascular Biology 36, suppl_1 (2016). http://dx.doi.org/10.1161/atvb.36.suppl_1.183.

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Background: Negative remodeling of extracellular matrix (ECM) is a key pathological feature associated with aortic dissections and aneurysms. Col V is a minor fibrillar collagen that incorporates into growing fibrils with Col I, and is involved in regulating the geometry and tensile strength of ECM. Col V normally exists as α 1 (V) 2 α 2 (V) 1 heterotrimers but may present as α 1 (V) 3 homotrimers in pathological tissues. To experimentally increase the existence of α 1 (V) 3 homotrimer, we deleted the Col5a2 gene, which encodes the α2(V) chain. Col5a2 +/- mice showed increased compliance and r
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Geng, Yong-Jian, Dongchun Guo, Dianna M. Milewicz, L. Maximillian Buja, Jinjie Wang, and Shuping Ge. "Abstract 2677: Reduction In Tie-2+/flk-1+ Vascular Stem Cells In Thoracic Aortic Aneurysm With Dissections: A Novel Contributor To Acellular Lesion Development." Circulation 116, suppl_16 (2007). http://dx.doi.org/10.1161/circ.116.suppl_16.ii_593-c.

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Background. Ascending thoracic aortic aneurysms leading to type A dissections (TAAD) are a life-threatening disease triggered by a complex interactions between environmental and genetic factors. Pathologically, this disease is characterized by a progressive loss of vascular smooth muscle cells (SMCs) and extracellular elastic fibers in the aortic media. Apoptosis, a form of programmed cell death, has been shown to contribute to the loss of medial SMCs. However, little is known about the role of vascular progenitor or stem cells in the pathogenesis of aortic aneurysms. Methods and Results. In t
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Riehle, Christian, Benjamin Wayment, Karla M. Pires, et al. "Abstract 3559: Insulin Receptor Substrates (IRS) Signaling are Essential Regulators of Mitochondrial Function and Cardiomyocyte Survival." Circulation 118, suppl_18 (2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_444-b.

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It has recently been reported that impaired PI3K signaling leads to cardiac mitochondrial dysfunction and that cardiac insulin receptor deficiency impairs cardiac growth. Signaling from insulin and insulin-like growth factor 1 receptors to PI3K is mediated by insulin receptor substrates (IRS) 1 and 2. Our objective was to determine the contribution of IRS isoforms on cardiac structure, mitochondrial and contractile function. For this purpose we generated mice with cardiomyocyte-specific deletion of IRS1 (CIRS1KO) or IRS2 (CIRS2KO) or IRS1 + IRS2 (CIRS12KO). While the single KOs had normal surv
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Andrade, Ana Cláudia De Souza, Laisa Marina Rosa Rey, Isabela Carvalho dos Santos, et al. "Cutaneous Asthenia in a Domestic Cat (Felis silvestris catus)." Acta Scientiae Veterinariae 49 (January 18, 2021). http://dx.doi.org/10.22456/1679-9216.110142.

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Background: Cutaneous asthenia or Ehlers-Danlos syndrome is an inherited and rare disease. This infirmity is from an autosomal mutation that influences the collagen synthesis of the carrier. Thus, its skeleton, formed of fibers, is structurally defective. The disease is characterized by hyperelasticity and skin fragility, leading to lesions throughout the skin. The lesions may manifest in specific places or in a generalized way, being more frequent in the limbs, neck, and back. This disease does not have a specific treatment, only management care to avoid new traumas.Case: A 3-year-old male ca
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Bowman, Marion Hofmann, Jeannine Wilk, Gene Kim, Yanmin Zhang, Jalees Rehman, and Elizabeth McNally. "Abstract 424: Vascular Smooth Muscle Cell Expression of S100a12 in Vivo Induces Enhanced Oxidative Stress & Vascular Remodeling." Circulation 118, suppl_18 (2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_302-d.

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S100A12 is a small calcium binding protein that is a signal transduction ligand of the receptor for advance glycation endproducts (RAGE). S100A12, like RAGE, is expressed in the vessel wall of atherosclerotic vasculature, particularly in smooth muscle cells (SMC). While RAGE has been extensively implicated in inflammatory states such as atherosclerosis, the role of S100A12 is less clear. We tested the hypothesis that expression of human S100A12 directly exacerbates vascular inflammation. Several lines of Bl6/J transgenic mice (tg) expressing human S100A12 in SMC under control of the SM22a prom
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Kwan, Eugene, elyar ghafoori, Wilson Good, et al. "Abstract 4136863: Diffuse Functional and Structural Abnormalities in Fibrosis: Potential Structural Basis for Sustaining Atrial Fibrillation." Circulation 150, Suppl_1 (2024). http://dx.doi.org/10.1161/circ.150.suppl_1.4136863.

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Background: Structural remodeling is associated with atrial fibrillation (AF), but detailed structural and functional characteristics is not well defined. Goal: Using a novel transgenic goat model with cardiac-specific overexpression of TGF-β1 leading to increased cardiac fibrosis, we evaluated detailed structural and functional differences between fibrotic and healthy regions of the atria. Methods: Ex-vivo MRI and histology were used to evaluate fibrosis, fiber disarray, and structural anisotropy. Ex-vivo MRI intensity values were scaled to standard deviations around the mean. The functional
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Melhoranse Gouveia, Bruna, Peter M. Ferguson, Serigne N. Lo, et al. "In vivo reflectance confocal microscopy role for early to advanced lentigo maligna melanoma spectrum: A systematic review and pooled analysis." Journal of the European Academy of Dermatology and Venereology, November 13, 2024. http://dx.doi.org/10.1111/jdv.20389.

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AbstractLentigo maligna (LM) is a growing problem worldwide and the main type of melanoma in situ in some Caucasian populations. It presents as a spectrum from atypical intraepidermal melanocytic proliferation (AIMP) to invasive lentigo maligna melanoma (LMM). Accurate diagnosis and staging are crucial for determining appropriate management strategies. To assess the role of in vivo reflectance confocal microscopy (RCM) in differentiating early and advanced stages of lentigo maligna. A systematic search was conducted on Medline, PubMed, Scopus, Web of Science, Proquest Central, Embase, Cochrane
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Kovacheva, Ekaterina, Tobias Gerach, Steffen Schuler, Marco Ochs, Olaf Dössel, and Axel Loewe. "Causes of altered ventricular mechanics in hypertrophic cardiomyopathy: an in-silico study." BioMedical Engineering OnLine 20, no. 1 (2021). http://dx.doi.org/10.1186/s12938-021-00900-9.

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Abstract Background Hypertrophic cardiomyopathy (HCM) is typically caused by mutations in sarcomeric genes leading to cardiomyocyte disarray, replacement fibrosis, impaired contractility, and elevated filling pressures. These varying tissue properties are associated with certain strain patterns that may allow to establish a diagnosis by means of non-invasive imaging without the necessity of harmful myocardial biopsies or contrast agent application. With a numerical study, we aim to answer: how the variability in each of these mechanisms contributes to altered mechanics of the left ventricle (L
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Jairo, Rodrı́guez-Padilla, Petras Argyrios, Magat Julie, Ozenne Valery, and Vigmond Edward. "Impact of Intraventricular Septal Fiber Orientation on Cardiac Electromechanical Function : Supplementary figures." April 19, 2022. https://doi.org/10.5281/zenodo.6469798.

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Supplementary figures S1, S2, and S3 of the following article Rodriguez Padilla J, Petras A, Magat J, Bayer J, Bihan-Poudec Y, El-Hamrani D, Ramlugun G, Neic A, Augustin C, Vaillant F, Constantin M, Benoist D, Pourtau L, Dubes V, Rogier J, Labrousse L, Bernus O, Quesson B, Haissaguerre M, Gsell M, Plank G, Ozenne V, Vigmond E. Impact of Intraventricular Septal Fiber Orientation on Cardiac Electromechanical Function. Am J Physiol Heart Circ Physiol. 2022 Mar 18 Epub ahead of print. PMID: 35302879. <strong>Legends of the supplementary figures.</strong> <strong>Figure S1. </strong>Helix angle as
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