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      Aluminum-Induced Entropy in Biological Systems: Implications for Neurological Disease

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          Abstract

          Over the last 200 years, mining, smelting, and refining of aluminum (Al) in various forms have increasingly exposed living species to this naturally abundant metal. Because of its prevalence in the earth's crust, prior to its recent uses it was regarded as inert and therefore harmless. However, Al is invariably toxic to living systems and has no known beneficial role in any biological systems. Humans are increasingly exposed to Al from food, water, medicinals, vaccines, and cosmetics, as well as from industrial occupational exposure. Al disrupts biological self-ordering, energy transduction, and signaling systems, thus increasing biosemiotic entropy. Beginning with the biophysics of water, disruption progresses through the macromolecules that are crucial to living processes (DNAs, RNAs, proteoglycans, and proteins). It injures cells, circuits, and subsystems and can cause catastrophic failures ending in death. Al forms toxic complexes with other elements, such as fluorine, and interacts negatively with mercury, lead, and glyphosate. Al negatively impacts the central nervous system in all species that have been studied, including humans. Because of the global impacts of Al on water dynamics and biosemiotic systems, CNS disorders in humans are sensitive indicators of the Al toxicants to which we are being exposed.

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          Central dogma of molecular biology.

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            The endothelial glycocalyx: composition, functions, and visualization

            This review aims at presenting state-of-the-art knowledge on the composition and functions of the endothelial glycocalyx. The endothelial glycocalyx is a network of membrane-bound proteoglycans and glycoproteins, covering the endothelium luminally. Both endothelium- and plasma-derived soluble molecules integrate into this mesh. Over the past decade, insight has been gained into the role of the glycocalyx in vascular physiology and pathology, including mechanotransduction, hemostasis, signaling, and blood cell–vessel wall interactions. The contribution of the glycocalyx to diabetes, ischemia/reperfusion, and atherosclerosis is also reviewed. Experimental data from the micro- and macrocirculation alludes at a vasculoprotective role for the glycocalyx. Assessing this possible role of the endothelial glycocalyx requires reliable visualization of this delicate layer, which is a great challenge. An overview is given of the various ways in which the endothelial glycocalyx has been visualized up to now, including first data from two-photon microscopic imaging.
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              LXXIII.—Oxidation of tartaric acid in presence of iron

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                Author and article information

                Journal
                J Toxicol
                J Toxicol
                JT
                Journal of Toxicology
                Hindawi Publishing Corporation
                1687-8191
                1687-8205
                2014
                2 October 2014
                : 2014
                : 491316
                Affiliations
                1Neural Dynamics Research Group, Department of Ophthalmology and Visual Sciences, 828 W. 10th Avenue, Vancouver, British Columbia, Canada V5Z 1L8
                2Program Experimental Medicine, University of British Columbia, Vancouver, Canada V5Z 1L8
                3Program in Neurosciences, University of British Columbia, Vancouver, Canada V5Z 1L8
                4MIT Computer Science and Artificial Intelligence Laboratory, 32 Vassar Street, Cambridge, MA 02139, USA
                5Hudson, FL 34667, USA
                6Department of Communicative Disorders, University of Louisiana, Lafayette, LA 70504-3170, USA
                7Internal Medicine Group Practice, PhyNet Inc., 4002 Technology Center, Longview, TX 75605, USA
                Author notes
                *Christopher A. Shaw: cashawlab@ 123456gmail.com

                Academic Editor: William Valentine

                Article
                10.1155/2014/491316
                4202242
                25349607
                408ef0f8-1a65-4aab-b1b5-0a217cb890fe
                Copyright © 2014 Christopher A. Shaw et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 9 June 2014
                : 28 July 2014
                Categories
                Review Article

                Toxicology
                Toxicology

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