32 research outputs found

    Barras de cereais contendo alto teor de proteína de soja e isoflavonas na avaliação do perfil lipídico de indivíduos dislipidêmicos.

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    A dislipidemia é um problema de saúde pública devido a sua estreita relação com doenças cardiovasculares. A partir disso, estratégias farmacológicas e não-farmacológicas têm sido aplicadas. Entre elas está o desenvolvimento de alimentos funcionais que visem modificação do perfil lipídico. A ANVISA permite a alegação: O consumo diário de no mínimo 25 g de proteína de soja pode ajudar a reduzir o colesterol. O objetivo deste trabalho foi desenvolver um alimento tipo barra de cereais, contendo basicamente ingredientes derivados de soja e utilizá-lo em estudo clínico com indivíduos dislipidêmicos, para avaliar o efeito sobre o perfil lipídico, glicose e índices antropométricos. METODOLOGIA: Foram feitos inúmeros testes em laboratório de combinações dos ingredientes de soja (flocos, proteína texturizada, proteína isolada e soja torrada natural) até atingir características sensoriais desejáveis e no mínimo 25 g de proteína e ± 80 mg de isoflavonas em 100g de produto. Foi coletado sangue, antes e após 45 dias de consumo de 3 barras de soja/dia, de 25 indivíduos com colesterol total (CT) >200 mg/dL ou TG> 150 mg/dL e maiores de 18 anos. As análises de CT, HDL, TG e glicose foram realizadas utilizando metodologia automatizada. O LDL foi calculado. Foram medidos circunferência abdominal, peso, altura, para cálculo do IMC. RESULTADOS: Obteve-se barras de soja com ±30 g de proteína e ±100 mg de isoflavonas em 100g de produto. Não houve diminuição significativa (p0,05) nos parâmetros avaliados. No entanto, houve uma tendência de diminuição do nível de TG (±13%) e aumento do HDL (± 7%) após 45 dias de consumo. CONCLUSÃO: É possível produzir barras de soja com alto teor de proteínas e isoflavonas. Seus efeitos sobre o perfil lipídico devem ser estudados por mais tempo e população maior, pois apresentaram ótimas tendências de regularização dos níveis de TG e HDL

    Oxidative stress and inflammatory markers are associated with depression and nicotine dependence

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    AbstractTo determine if oxidative stress and inflammation are linked with major depressive disorder, nicotine dependence and both disorders combined. This study comprised 150 smokers and 191 never smokers. The instruments were: a socio-demographic questionnaire, diagnoses of mood disorder and nicotine dependence according to DSM-IV, (SCID-IV), and the Alcohol, Smoking and Substance Involvement Screening Test. Laboratory assessments included: nitric oxide metabolites (NOx), lipid hydroperoxides, malondialdehyde (MDA), total reactive antioxidant potential (TRAP), advanced oxidation protein products (AOPP), fibrinogen concentrations, homocysteine, erythrocytes sedimentation rate (ESR) and high-sensitivity C-reactive protein (hs-CRP) were assayed from blood specimens. Statistically significant differences were found among depressed smokers who had more severe depressive symptoms, a higher risk of alcohol consumption, more suicide attempts, and more disability for work than non-depressed never smokers. Depressed smokers had significantly higher levels of NOx, fibrinogen, hs-CRP, AOPP, ESR and lower levels of TRAP compared to non-depressed never smokers. Depressed smokers had significant levels of oxidative stress and inflammatory biomarkers after adjusting for gender, age, years of education, disability for work, and laboratory measures. The levels of NOx, lipid hydroperoxides, AOPP, and fibrinogen were substantially higher, whereas levels of TRAP were lower in depressed smokers compared to non-depressed never smokers. (1) Depressed smokers exhibited altered concentrations of NOx, lipid hydroperoxides, AOPP, TRAP, and fibrinogen. (2) Depressed smokers were more unable to work, showed more severe depressive symptoms and attempted suicide more frequently

    The Therapeutic Potential of Mangosteen Pericarp as an Adjunctive Therapy for Bipolar Disorder and Schizophrenia

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    New treatments are urgently needed for serious mental illnesses including bipolar disorder and schizophrenia. This review proposes that Garcinia mangostana Linn. (mangosteen) pericarp is a possible adjunctive therapeutic agent for these disorders. Research to date demonstrates that neurobiological properties of the mangosteen pericarp are well aligned with the current understanding of the pathophysiology of bipolar disorder and schizophrenia. Mangosteen pericarp has antioxidant, putative neuroprotective, anti-inflammatory, and putative mitochondrial enhancing properties, with animal studies demonstrating favorable pharmacotherapeutic benefits with respect to these disorders. This review summarizes evidence of its properties and supports the case for future studies to assess the utility of mangosteen pericarp as an adjunctive treatment option for mood and psychotic disorders

    Neurobiological mechanisms linking obesity and depression

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    Can endolysosomal deacidification and inhibition of autophagy prevent severe COVID-19?

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    The possibility is examined that immunomodulatory pharmacotherapy may be clinically useful in managing the pandemic coronavirus disease 2019 (COVID-19), known to result from infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive-sense single-stranded RNA virus. The dominant route of cell entry of the coronavirus is via phagocytosis, with ensconcement in endosomes thereafter proceeding via the endosomal pathway, involving transfer from early (EEs) to late endosomes (LEs) and ultimately into lysosomes via endolysosomal fusion. EE to LE transportation is a rate-limiting step for coronaviruses. Hence inhibition or dysregulation of endosomal trafficking could potentially inhibit SARS-CoV-2 replication. Furthermore, the acidic luminal pH of the endolysosomal system is critical for the activity of numerous pH-sensitive hydrolytic enzymes. Golgi sub-compartments and Golgi-derived secretory vesicles also depend on being mildly acidic for optimal function and structure. Activation of endosomal toll-like receptors by viral RNA can upregulate inflammatory mediators and contribute to a systemic inflammatory cytokine storm, associated with a worsened clinical outcome in COVID-19. Such endosomal toll-like receptors could be inhibited by the use of pharmacological agents which increase endosomal pH, thereby reducing the activity of acid-dependent endosomal proteases required for their activity and/or assembly, leading to suppression of antigen-presenting cell activity, decreased autoantibody secretion, decreased nuclear factor-kappa B activity and decreased pro-inflammatory cytokine production. It is also noteworthy that SARS-CoV-2 inhibits autophagy, predisposing infected cells to apoptosis. It is therefore also suggested that further pharmacological inhibition of autophagy might encourage the apoptotic clearance of SARS-CoV-2-infected cells

    Preventing the development of severe COVID-19 by modifying immunothrombosis

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    BACKGROUND: COVID-19-associated acute respiratory distress syndrome (ARDS) is associated with significant morbidity and high levels of mortality. This paper describes the processes involved in the pathophysiology of COVID-19 from the initial infection and subsequent destruction of type II alveolar epithelial cells by SARS-CoV-2 and culminating in the development of ARDS. MAIN BODY: The activation of alveolar cells and alveolar macrophages leads to the release of large quantities of proinflammatory cytokines and chemokines and their translocation into the pulmonary vasculature. The presence of these inflammatory mediators in the vascular compartment leads to the activation of vascular endothelial cells platelets and neutrophils and the subsequent formation of platelet neutrophil complexes. These complexes in concert with activated endothelial cells interact to create a state of immunothrombosis. The consequence of immunothrombosis include hypercoagulation, accelerating inflammation, fibrin deposition, migration of neutrophil extracellular traps (NETs) producing neutrophils into the alveolar apace, activation of the NLRP3 inflammazome, increased alveolar macrophage destruction and massive tissue damage by pyroptosis and necroptosis Therapeutic combinations aimed at ameliorating immunothrombosis and preventing the development of severe COVID-19 are discussed in detail
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