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Books on the topic 'Elastic tissue'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Derek, Chadwick, Goode Jamie, Ciba Foundation, and Symposium on the Molecular Biology and Pathology of Elastic Tissues (1994 : Nairobi, Kenya), eds. The molecular biology and pathology of elastic tissues. Chichester: J. Wiley, 1995.

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2

Miller, James Stuart. A particle-based approach to elastic tissue modelling. Manchester: University ofManchester, 1996.

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3

Ladislas, Robert, and Hornebeck William 1946-, eds. Elastin and elastases. Boca Raton, Fla: CRC Press, 1989.

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4

Chadwick, Derek J., and Jamie A. Goode, eds. Ciba Foundation Symposium 192 - The Molecular Biology and Pathology of Elastic Tissues. Chichester, UK: John Wiley & Sons, Ltd., 1995. http://dx.doi.org/10.1002/9780470514771.

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5

Hasegawa, Hideyuki. Ultrasonic methods for measurement of small motion and deformation of biological tissues for assessment of viscoelasticity. New York, NY, USA: ASME, 2014.

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6

Sandberg, L. Elastin and Elastic Tissue. Springer London, Limited, 2012.

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7

Sandberg, L. Elastin and Elastic Tissue. Springer, 2012.

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8

Elastic Fiber Matrices: Biomimetic Approaches to Regeneration and Repair. CRC Press LLC, 2016.

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9

Elastic Fiber Matrices: Biomimetic Approaches to Regeneration and Repair. Taylor & Francis Group, 2016.

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10

Ramamurthi, Anand, and Chandrasekhar Kothapalli. Elastic Fiber Matrices: Biomimetic Approaches to Regeneration and Repair. Taylor & Francis Group, 2018.

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11

Ramamurthi, Anand, and Chandrasekhar Kothapalli. Elastic Fiber Matrices: Biomimetic Approaches to Regeneration and Repair. Taylor & Francis Group, 2018.

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12

Ramamurthi, Anand, and Chandrasekhar Kothapalli. Elastic Fiber Matrices: Biomimetic Approaches to Regeneration and Repair. Taylor & Francis Group, 2018.

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13

Ramamurthi, Anand, and Chandrasekhar Kothapalli. Elastic Fiber Matrices: Biomimetic Approaches to Regeneration and Repair. Taylor & Francis Group, 2018.

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14

Symposium, CIBA Foundation, Jamie A. Goode, and Derek J. Chadwick. Molecular Biology and Pathology of Elastic Tissues. Wiley & Sons, Limited, John, 2007.

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15

Goode, Jamie A., and Derek J. Chadwick. Molecular Biology and Pathology of Elastic Tissues. Wiley & Sons, Incorporated, John, 2008.

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16

Aguilar-Torres, Río. Assessment of left atrial function. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0010.

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The left atrium (LA) plays an important role in cardiovascular performance, not only as a mechanical contributor, elastic reservoir, and a primer for left ventricular filling, but also as a participant in the regulation of intravascular volume through the production of atrial natriuretic peptide.Although LA diameter in the parasternal long-axis view has been routinely employed, LA volume is a more robust marker for predicting events than LA areas or diameters. The assessment of LA performance based on two-dimensional volumetrics, Doppler evaluation of mitral, pulmonary vein flow, and annular tissue Doppler, as well as deformation imaging techniques, may provide incremental information for prognostic purposes and for the evaluation of severity and duration of conditions associated with LA overload.The aims of this chapter are to explain the basics of LA function, and to describe the role of Doppler echocardiography techniques, and how to implement them, for the non-invasive evaluation of LA in clinical practice.

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17

Robert, L., and M. Moczar. Methods of Connective Tissue Research (Frontiers of Matrix Biology, Vol 10). S. Karger AG (Switzerland), 1985.

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18

Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.

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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.

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19

Vanakker, Olivier M., ed. Soft tissue mineralization: an enlarging disease spectrum with pseudoxanthoma elasticum as paradigm. Frontiers Media SA, 2014. http://dx.doi.org/10.3389/978-2-88919-209-0.

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20

Poppinga, Simon, Ulrike Bauer, Thomas Speck, and Alexander G. Volkov. Motile traps. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198779841.003.0014.

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We review the biomechanics, functional morphology, and physiology of motile traps. The movements of snap traps in Aldrovanda and Dionaea, motile adhesive traps in Drosera and Pinguicula, and suction traps in Utricularia are driven by active water displacement processes leading to reversible turgor changes of motor cells, irreversible growth, or mechanical pre-stressing of tissues. In some cases, the motion is amplified by the release of elastic energy stored in these tissues. The only known case of a passive motile trapping movement is the ‘springboard’ trapping mechanism of Nepenthes gracilis, in which a rapid vibration of the pitcher lid is actuated by the impact force of raindrops. Open research questions are summarized and future studies are suggested.

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21

Kanai, Hiroshi, and Hideyuki Hasegawa. Ultrasonic Methods for Measurement of Small Motion and Deformation of Biological Tissues for Assessment of Viscoelasticity. Momentum Press, 2014.

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22

MacGrogan, Donal, José Maria Pérez-Pomares, Bill Chaudhry, José Luis de la Pompa, and Deborah J. Henderson. From cushions to leaflets: morphogenesis of cardiac atrioventricular valves. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0017.

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At the looping stage of heart development, tissue patterning of myocardium and endocardium at the atrioventricular (AV) junction defines a morphogenic field competent to form valves that initially appear as protrusions of proteoglycan-rich extracellular matrix (ECM) called endocardial cushions (ECs) which are cellularized by an endocardial-mesenchymal transition (EMT). Cellular proliferation results in fusion of the major AV mesenchymal cushions and AV septation, whereas smaller cushions receive a supply from epicardially derived cells. These various sources of mesenchyme precursors give rise to most of the valve structures, leaflets, annuli, and supporting tension apparatus. During valve leaflet maturation, the ECM matrix accumulates collagen and elastin and assembles into a thin flexible fibrous structure, which is remarkably tough. Valve development is regulated by the cross-talk between developmental signalling pathways. Pathogenic mutations in a subset of developmentally important genes have been linked to valve disease, suggesting that developmental defects may underlie valve disease in adulthood.

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