57 research outputs found

    Prevenção de quedas nos idosos

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    Esta webaula contempla os principais aspectos na prevenção de quedas nos idosos

    Treino prevenção de quedas

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    Este livro digital contém um programa de exercícios domiciliares para prevenção de quedas nos idosos baseado no programa de exercícios domiciliares de Otago

    Orientações de prevenção de quedas no domicílio

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    Este folder contém orientações de prevenção de quedas no domicílio. Também divulga informações sobre o aplicativo "Não deixe a vovó cair" que está disponível gratuitamente na loja Google Play

    Não deixe a vovó cair

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    Infográfico contendo informações e orientações para a prevenção de quedas em idosos

    Fatores de risco para quedas na velhice

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    Infográfico contendo informações sobre os principais fatores de risco para quedas em idosos

    Cuidados paliativos

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    Cuidado paliativo é uma abordagem que promove a qualidade de vida de pacientes e seus familiares que enfrentam doenças que ameacem a continuidade da vida, por meio da prevenção e alívio do sofrimento. Este livro digital contempla informações sobre os cuidados paliativos, suas indicações e aplicações

    Exercício físico para idosos

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    Infográfico com informações sobre as diferentes modalidades e tipos de exercícios indicados para os idosos

    O idoso caiu e agora? O que fazer após uma queda

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    Infográfico contendo informações e orientações sobre como o idoso deve agir após uma queda

    Photosensitized Membrane Permeabilization Requires Contact-Dependent Reactions between Photosensitizer and Lipids.

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    Although the general mechanisms of lipid oxidation are known, the chemical steps through which photosensitizers and light permeabilize lipid membranes are still poorly understood. Herein we characterized the products of lipid photooxidation and their effects on lipid bilayers, also giving insight into their formation pathways. Our experimental system was designed to allow two phenothiazinium-based photosensitizers (methylene blue, MB, and DO15) to deliver the same amount of singlet oxygen molecules per second to 1-palmitoyl-2-oleoyl- sn-glycero-3-phosphocholine liposome membranes, but with a substantial difference in terms of the extent of direct physical contact with lipid double bonds; that is, DO15 has a 27-times higher colocalization with ω-9 lipid double bonds than MB. Under this condition, DO15 permeabilizes membranes at least 1 order of magnitude more efficiently than MB, a result that was also valid for liposomes made of polyunsaturated lipids. Quantification of reaction products uncovered a mixture of phospholipid hydroperoxides, alcohols, ketones, and aldehydes. Although both photosensitizers allowed the formation of hydroperoxides, the oxidized products that require direct reactions between photosensitizer and lipids were more prevalent in liposomes oxidized by DO15. Membrane permeabilization was always connected with the presence of lipid aldehydes, which cause a substantial decrease in the Gibbs free energy barrier for water permeation. Processes depending on direct contact between photosensitizers and lipids were revealed to be essential for the progress of lipid oxidation and consequently for aldehyde formation, providing a molecular-level explanation of why membrane binding correlates so well with the cell-killing efficiency of photosensitizers

    Central Role of Pyrophosphate in Acellular Cementum Formation

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    Background: Inorganic pyrophosphate (PPi) is a physiologic inhibitor of hydroxyapatite mineral precipitation involved in regulating mineralized tissue development and pathologic calcification. Local levels of PPi are controlled by antagonistic functions of factors that decrease PPi and promote mineralization (tissue-nonspecific alkaline phosphatase, Alpl/TNAP), and those that increase local PPi and restrict mineralization (progressive ankylosis protein, ANK; ectonucleotide pyrophosphatase phosphodiesterase-1, NPP1). The cementum enveloping the tooth root is essential for tooth function by providing attachment to the surrounding bone via the nonmineralized periodontal ligament. At present, the developmental regulation of cementum remains poorly understood, hampering efforts for regeneration. To elucidate the role of PPi in cementum formation, we analyzed root development in knock-out ((-/-)) mice featuring PPi dysregulation. Results: Excess PPi in the Alpl(-/-) mouse inhibited cementum formation, causing root detachment consistent with premature tooth loss in the human condition hypophosphatasia, though cementoblast phenotype was unperturbed. Deficient PPi in both Ank and Enpp1(-/-) mice significantly increased cementum apposition and overall thickness more than 12-fold vs. controls, while dentin and cellular cementum were unaltered. Though PPi regulators are widely expressed, cementoblasts selectively expressed greater ANK and NPP1 along the root surface, and dramatically increased ANK or NPP1 in models of reduced PPi output, in compensatory fashion. In vitro mechanistic studies confirmed that under low PPi mineralizing conditions, cementoblasts increased Ank (5-fold) and Enpp1 (20-fold), while increasing PPi inhibited mineralization and associated increases in Ank and Enpp1 mRNA. Conclusions: Results from these studies demonstrate a novel developmental regulation of acellular cementum, wherein cementoblasts tune cementogenesis by modulating local levels of PPi, directing and regulating mineral apposition. These findings underscore developmental differences in acellular versus cellular cementum, and suggest new approaches for cementum regeneration
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