Importância da comunicação e do aconselhamento de dermofarmácia e cosmética em peles sensíveis

A aparência física e os cuidados inerentes à mesma apresentam-se como uma preocupação crescente do indivíduo. Desta forma, o aconselhamento em dermofarmácia e cosmética tem ganho relevância. A pele sensível, tratando-se de um estado de pele, carateriza-se por uma reação inflamatória, que afeta a integridade da barreira cutânea. Torna-se fundamental que os profissionais de farmácia se encontrem aptos para aconselhar e comunicar da melhor forma. Delinear e implementar uma ação de formação sobre comunicação em saúde, no contexto do aconselhamento de dermofarmácia e cosmética em peles sensíveis.info:eu-repo/semantics/publishedVersio

Decreased Proteolytic Activity of the Mitochondrial Amyloid-β Degrading Enzyme, PreP Peptidasome, in Alzheimer's Disease Brain Mitochondria

This is the published version. Copyright 2011 by Journal of Alzheimer's Disease.Accumulation of amyloid-β peptide (Aβ), the neurotoxic peptide implicated in the pathogenesis of Alzheimer's disease (AD), has been shown in brain mitochondria of AD patients and of AD transgenic mouse models. The presence of Aβ in mitochondria leads to free radical generation and neuronal stress. Recently, we identified the presequence protease, PreP, localized in the mitochondrial matrix in mammalian mitochondria as the novel mitochondrial Aβ-degrading enzyme. In the present study, we examined PreP activity in the mitochondrial matrix of the human brain's temporal lobe, an area of the brain highly susceptible to Aβ accumulation and reactive oxygen species (ROS) production. We found significantly lower hPreP activity in AD brains compared with non-AD age-matched controls. By contrast, in the cerebellum, a brain region typically spared from Aβ accumulation, there was no significant difference in hPreP activity when comparing AD samples to non-AD controls. We also found significantly reduced PreP activity in the mitochondrial matrix of AD transgenic mouse brains (Tg mAβPP and Tg mAβPP/ABAD) when compared to non-transgenic aged-matched mice. Furthermore, mitochondrial fractions isolated from AD brains and Tg mAβPP mice had higher levels of 4-hydroxynonenal, an oxidative product, as compared with those from non-AD and nonTg mice. Accordingly, activity of cytochrome c oxidase was significantly reduced in the AD mitochondria. These findings suggest that decreased PreP proteolytic activity, possibly due to enhanced ROS production, contributes to Aβ accumulation in mitochondria leading to the mitochondrial toxicity and neuronal death that is exacerbated in AD. Clearance of mitochondrial Aβ by PreP may thus be of importance in the pathology of AD

a protocol for a self-care intervention

Funding Information: This project was supported by the Comprehensive Health Research Centre (CHRC) with registered number NCT06235593 . Funding Information: This work is funded by nationalfunds through the Foundation for Science and Technology, under the project UIDP/04923/2020. Publisher Copyright: © 2024Most aging populations report chronic illnesses, which are usually permanent or recurrent, significantly affect well-being and quality of life, require daily and consistent healthcare management, and last more than three months. Improved health outcomes and reduced healthcare costs are associated with self-care in treating chronic illnesses. The aim is to describe a protocol using a self-care intervention in a person with a chronic disease. A longitudinal study will be conducted with 40 patients. This article describes a protocol for a self-care intervention in a person with a chronic disease. The outcome measures will be compared with measures after the intervention in three different chronologic times. Randomization will be used to assign participants to the intervention group. The present study is expected to generate significant information about the role of self-care intervention in persons with chronic disease.publishersversionpublishe

Mitochondrial hypermetabolism precedes impaired autophagy and synaptic disorganization in App knock-in Alzheimer mouse models.

Accumulation of amyloid β-peptide (Aβ) is a driver of Alzheimer's disease (AD). Amyloid precursor protein (App) knock-in mouse models recapitulate AD-associated Aβ pathology, allowing elucidation of downstream effects of Aβ accumulation and their temporal appearance upon disease progression. Here we have investigated the sequential onset of AD-like pathologies in AppNL-F and AppNL-G-F knock-in mice by time-course transcriptome analysis of hippocampus, a region severely affected in AD. Strikingly, energy metabolism emerged as one of the most significantly altered pathways already at an early stage of pathology. Functional experiments in isolated mitochondria from hippocampus of both AppNL-F and AppNL-G-F mice confirmed an upregulation of oxidative phosphorylation driven by the activity of mitochondrial complexes I, IV and V, associated with higher susceptibility to oxidative damage and Ca2+-overload. Upon increasing pathologies, the brain shifts to a state of hypometabolism with reduced abundancy of mitochondria in presynaptic terminals. These late-stage mice also displayed enlarged presynaptic areas associated with abnormal accumulation of synaptic vesicles and autophagosomes, the latter ultimately leading to local autophagy impairment in the synapses. In summary, we report that Aβ-induced pathways in App knock-in mouse models recapitulate key pathologies observed in AD brain, and our data herein adds a comprehensive understanding of the pathologies including dysregulated metabolism and synapses and their timewise appearance to find new therapeutic approaches for AD

Avaliação estato-ponderal e da actividade física numa amostra representativa da população adulta portuguesa

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Caracterização estato-ponderal de crianças e adolescentes numa amostra representativa da população portuguesa

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Determinantes da saúde e escolha alimentar em idosos portugueses

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Avaliação do aporte energético e nutricional e sua relação com dados antropométricos dos idosos portugueses

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