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Books on the topic 'Fibrils'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Otzen, Daniel Erik, ed. Amyloid Fibrils and Prefibrillar Aggregates. Wiley-VCH Verlag GmbH & Co. KGaA, 2013. http://dx.doi.org/10.1002/9783527654185.

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2

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Silica, some silicates, coal dust and para-Aramid fibrils. IARC, 1997.

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3

Bock, Gregory R., and Jamie A. Goode, eds. Ciba Foundation Symposium 199 - The Nature and Origin of Amyloid Fibrils. John Wiley & Sons, Ltd., 1996. http://dx.doi.org/10.1002/9780470514924.

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4

Delmonte, John. Technology of carbon and graphite fiber composites. R.E. Krieger Pub. Co., 1987.

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5

Sidney, Mindess, ed. Fibre reinforced cementitious composites. Elsevier Applied Science, 1990.

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6

Sidney, Mindess, ed. Fibre reinforced cementitious composites. 2nd ed. Taylor & Francis, 2007.

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7

Calvin, Woodings, and Textile Institute (Manchester England), eds. Regenerated cellulose fibres. CRC Press, 2001.

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8

M, Gammon Luther, ed. Optical microscopy of fiber reinforced composites. ASM International, 2010.

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9

International Conference on Woodfiber-Plastic Composites (8th 2005 Madison, Wis.). Eighth International Conference on Woodfiber-Plastic Composites (and other natural fibers): May 23-25, 2005, Monona Terrace Community & Convention Center, Madison, Wisconsin, USA. Forest Products Society, 2005.

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10

Piggott, Michael R. Load bearing fibre composites. 2nd ed. MERP Enhanced Composites, 2001.

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11

Linda, Shuker, and Medical Research Council (Great Britain). Institute for Environment and Health., eds. Fibrous materials in the environment: A review of asbestos and man-made mineral fibres. MRC Institute for Environment and Health, 1997.

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12

Segars, James H., ed. Fibroids. John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118456996.

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13

Segars, James. Fibroids. John Wiley & Sons, 2013.

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14

United States. Food and Drug Administration. Office of Women's Health. Fibroids. FDA Office of Women's Health, 2007.

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15

Friederike, Behringer, ed. Demonstrationszentren für Faserverbundkunststoffe: Ergebnisse der Begleitforschung. Duncker & Humblot, 1995.

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16

Alonso, Javier Gonzalez. Fibras. J. Pastor, 1994.

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17

Leiris, Michel. Fibrils. Yale University Press, 2019. http://dx.doi.org/10.12987/9780300227857.

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18

Amyloid Fibrils And Prefibrillar Aggregates. Wiley-VCH Verlag GmbH, 2013.

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19

Galzitskaya, Oxana V., and Vijay Kumar. Structural Biology of Amyloid Fibrils. Elsevier Science & Technology Books, 2023.

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20

Galzitskaya, Oxana V. Structural Biology of Amyloid Fibrils. Elsevier Science & Technology, 2023.

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21

Symposium, CIBA Foundation, Jamie A. Goode, and Gregory R. Bock. Nature and Origin of Amyloid Fibrils. Wiley & Sons, Limited, John, 2007.

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22

Goode, Jamie A., and Gregory R. Bock. Nature and Origin of Amyloid Fibrils. Wiley & Sons, Incorporated, John, 2008.

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23

Costa, Pedro. Nature and Origin of Amyloid Fibrils. Wiley & Sons, Incorporated, John, 2008.

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24

Fibrils: The Rules of the Game. Yale University Press, 2017.

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25

The nature and origin of amyloid fibrils. Wiley, 1996.

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26

The Nature and Origin of Amyloid Fibrils. John Wiley & Sons, 1996.

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27

Otzen, Daniel Erik. Amyloid Fibrils and Prefibrillar Aggregates: Molecular and Biological Properties. Wiley & Sons, Incorporated, John, 2013.

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28

Otzen, Daniel Erik. Amyloid Fibrils and Prefibrillar Aggregates: Molecular and Biological Properties. Wiley & Sons, Limited, John, 2013.

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29

Otzen, Daniel Erik. Amyloid Fibrils and Prefibrillar Aggregates: Molecular and Biological Properties. Wiley & Sons, Incorporated, John, 2013.

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30

Otzen, Daniel Erik. Amyloid Fibrils and Prefibrillar Aggregates: Molecular and Biological Properties. Wiley & Sons, Incorporated, John, 2013.

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31

Guillery, Ray. Comparative anatomical studies of the hypothalamus that led to studies of thalamic synapses. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198806738.003.0007.

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The first part of this chapter illustrates the role of serendipity in science. We started a comparative project to understand the differences between reptiles and mammals in terms of their hypothalamic pathways; these studies of reptilian brains revealed tiny fibrillar rings present in axon terminals of lizards kept at low temperatures but absent in those kept warmer. These temperature-dependent fibrillar increases resembled changes seen in some synaptic terminals after their axons have been cut, so we briefly turned our attention to the changing appearances of the fibrils. Mammalian optic ner

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32

Mittal, Sajjan. Amyloidosis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0181.

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Amyloidosis is a multisystem disease caused by the extracellular deposition of insoluble abnormal fibrils that injure tissues and organs. The fibrils are formed by the aggregation of misfolded, normally soluble proteins. Systemic amyloid light-chain (AL) amyloidosis (primary amyloidosis) is the commonest type of amyloidosis in the developed world, accounting for 80% of cases. The remainder are due to AA amyloidosis (secondary or reactive amyloidosis), familial amyloidosis, or other rare types of amyloidosis. The most common clinical features at diagnosis are nephrotic syndrome, heart failure (

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33

(Contributor), WHO, ed. Silica, Some Silicates, Coal Dust and para-Aramid Fibrils (Iarc Monographs No. 68). World Health Organisation, 1997.

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34

Korbet, Stephen M., Melvin M. Schwartz, and Edmund J. Lewis. Fibrillary and immunotactoid glomerulopathy. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0081.

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Fibrillary or immunotactoid nephropathy is a rare deposition disease of unknown cause in which highly organized deposits containing immunoglobulin and complement are found in the glomerular basement membrane and mesangium. These deposits are not amyloid fibrils and do not stain with Congo red. They are usually polyclonal and are not associated with monoclonal paraproteins, or with cryoglobulins or systemic lupus, distinguishing them from other non-amyloid fibrillary glomerulopathies. There is debate about whether there is a useful distinction between distinct fibrillary and rarer immunotactoid

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35

Lachmann, Helen J., and Giampaolo Merlini. The patient with amyloidosis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0152.

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Amyloidosis is a disorder of protein folding in which normally soluble plasma proteins are deposited in the extracellular space in an abnormal insoluble fibrillar form. The process of amyloid formation and deposition causes cytotoxicity and progressive organ dysfunction. Amyloid is remarkably diverse and can be hereditary or acquired, localized or systemic, and lethal or merely an incidental finding. The most important numerically are AL amyloidosis, in which the fibrils are composed of monoclonal immunoglobulin light chains, and AA amyloidosis, in which the acute phase reactant Serum Amyloid

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36

Mendler, Markus. The heterotypic nature of cartilage fibrils: Ultrastructural localization of collagen types II, IX and XI. 1988.

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37

Kiel, Universität, ed. Effect of structural changes of collagen fibrils on bonding durability of luting resins to human dentin. 2005.

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38

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its a

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39

Ecerova, Zuzana. Assessment of type I collagen fibrils assembled in vitro in the presence of glucosamines using atomic force microscopy. 2004.

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40

Fiber-Reinforced Cements and Concretes (Advances in Concrete Technology). Taylor & Francis, 2000.

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41

Wetzel, Ronald, and Rakesh Mishra. Structural Biology. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0012.

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The 3,144–amino acid huntingtin protein (HTT) folds in water into a structure consisting of compact, organized domains interspersed with intrinsically disordered protein (IDP) elements. The IDPs function as sites of post-translational modifications and proteolysis as well as in targeting, binding, and aggregation. Although the dominant structural motif of HTT is the α‎-helix–rich HEAT repeat, the expanded polyglutamine (polyQ) toxicity responsible for Huntington’s disease is most likely played out within intrinsically disordered HTT exon 1–like fragments consisting of the 16– to 17–amino acid

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42

Alberton, Paolo. Investigation of the role of tenomodulin in the tendon stem cell niche, and in the regulation of the collagen fibrils upon mechanical stimulation. 2013.

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43

Govindan, Ramakrishnan, and Mohamed Zakriya. Natural Fiber Composites: Manufacturing, Characterization and Testing. Taylor & Francis Group, 2020.

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44

Natural Fiber Composites: Manufacturing, Characterization and Testing. Taylor & Francis Group, 2020.

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45

Govindan, Ramakrishnan, and Mohamed Zakriya G. Natural Fiber Composites: Manufacturing, Characterization and Testing. Taylor & Francis Group, 2022.

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46

Govindan, Ramakrishnan, and Mohamed Zakriya G. Natural Fiber Composites: Manufacturing, Characterization and Testing. Taylor & Francis Group, 2020.

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47

Govindan, Ramakrishnan, and Mohamed Zakriya G. Natural Fiber Composites: Manufacturing, Characterization and Testing. Taylor & Francis Group, 2020.

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48

Govindan, Ramakrishnan, and Mohamed Zakriya G. Natural Fiber Composites: Manufacturing, Characterization and Testing. Taylor & Francis Group, 2020.

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49

Ronco, Pierre M. Kidney involvement in plasma cell dyscrasias. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0150.

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Monoclonal proliferations of the B-cell lineage are characterized by abnormal and uncontrolled expansion of a single clone of B cells at different maturation stages, with a variable degree of differentiation to immunoglobulin-secreting plasma cells. Therefore, they are usually associated with the production and secretion in blood of a monoclonal immunoglobulin and/or a fragment thereof which may become deposited in tissues. These deposits can take the form of casts (in myeloma cast nephropathy), crystals (in myeloma-associated Fanconi syndrome), fibrils (in light-chain and exceptional heavy-ch

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50

Hon, DavidN S. Chemical Modification of Lignocellulosic Materials. CRC Press LLC, 2017.

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