1,406 research outputs found

    Building instrument to assess user satisfaction in communicating with health professionals based on the consensus of the Delphi method

    Get PDF
    Recent research in user-health professionals communication have emphasized the need to develop new instruments to evaluate user satisfaction in communicating with health professionalsinfo:eu-repo/semantics/publishedVersio

    UCP2 and ANT differently modulate proton-leak in brain mitochondria of long-term hyperglycemic and recurrent hypoglycemic rats

    Get PDF
    A growing body of evidence suggests that mitochondrial proton-leak functions as a regulator of reactive oxygen species production and its modulation may limit oxidative injury to tissues. The main purpose of this work was to characterize the proton-leak of brain cortical mitochondria from long-term hyperglycemic and insulininduced recurrent hypoglycemic rats through the modulation of the uncoupling protein 2 (UCP2) and adenine nucleotide translocator (ANT). Streptozotocin-induced diabetic rats were treated subcutaneously with twice-daily insulin injections during 2 weeks to induce the hypoglycemic episodes. No differences in the basal proton-leak, UCP2 and ANT protein levels were observed between the experimental groups. Mitochondria from recurrent hypoglycemic rats presented a decrease in proton-leak in the presence of GDP, a specific UCP2 inhibitor, while an increase in proton-leak was observed in the presence of linoleic acid, a proton-leak activator, this effect being reverted by the simultaneous addition of GDP. Mitochondria from longterm hyperglycemic rats showed an enhanced susceptibility to ANT modulation as demonstrated by the complete inhibition of basal and linoleic acid-induced proton-leak caused by the ANT specific inhibitor carboxyatractyloside. Our results show that recurrent-hypoglycemia renders mitochondria more susceptible to UCPs modulation while the protonleak of long-term hyperglycemic rats is mainly modulated by ANT, which suggest that brain cortical mitochondria have distinct adaptation mechanisms in face of different metabolic insults.The authors’ work is supported by the Fundação para a Ciência e a Tecnologia (FCT) (PTDC/SAU-NEU/103325/2008) co-funded by Fundo Europeu de Desenvolvimento Regional (FEDER) via Programa Operacional Factores de Competitividade (COMPETE). Susana Cardoso has a PhD fellowship from the Portuguese Foundation for Science and Technology (SFRH/BD/43968/2008)

    The Effect of Auriculotherapy on Situational Anxiety Trigged by Examinations: A Randomized Pilot Trial.

    Get PDF
    Auriculotherapy may activate the parasympathetic nerve system and reduce anxiety levels. Short-term auriculotherapy's effects and safety on university students' anxiety levels was assessed prior to exams. Methods A randomized, controlled pilot trial was conducted. The day before the exam, university students were randomly allocated to the auriculotherapy group (AA, n = 13) or the waiting-list group (WG, n = 13). Baseline measures were taken 4 weeks before the exam at Time point (TP 0); at 7.30 a.m. on the day before the exam (TP I); at 11 a.m. before auriculotherapy (TP II); 30 min after AA (TP III); and at 7.30 a.m. before the exam (TP IV). The outcomes were the State-Trait-Anxiety Inventory (STAI); quality of night-sleep, Visual Analogue scale (VAS) for anxiety, and salivary cortisol. Adverse events were also recorded.Results A total of 26 students participated in this study and became more anxious as assessed by STAI in TPII (p = 0.002) and TPIV (p = 0.000) than TP0. AA reduced the STAI in TPIII (p = 0.045) and PIV (p = 0.001) and the VAS (p = 0.012) in TPIV. Cortisol was reduced in TPIII (p = 0.004), and the AA slept better (p = 0.014) at TPIV. Discomfort at the auricular site was reported in only one AA participant.Conclusions Auriculotherapy appeared safe and effective in reducing anxiety levels before university exams

    MECANISMOS MOLECULARES SUBJACENTES AO CATABOLISMO MUSCULAR PROMOVIDO PELA DOXORRUBICINA

    Get PDF
    Chemotherapeutic agents like doxorubicin (DOX) are the foundation for the treatment of a variety of malignancies; however, these therapies have several side-effects. DOX may trigger or potentiate the muscle wasting observed in cancer patients, which is particularly worrying in frail old patients. Therefore, it is important to comprehend the mechanisms responsible for DOX-induced toxicity in skeletal muscle, to identify therapeutic targets envisioning the improvement of survival rates and quality of life of these patients. Hence, this review discusses the molecular players that may be involved in DOX-induced muscle wasting. From the analysis performed herein, DOX seems to induce the activation of the proteolytic ubiquitin proteasome pathway (UPP), which in turn can also be enhanced by DOX-induced increase in myostatin and tumor necrosis factor (TNF)-α signaling pathways, as well as insulin resistance. Furthermore, DOX-induced oxidative stress and mitochondrial dysfunction may also be critical contributors for muscle wasting. All these mechanisms may contribute to the loss of skeletal muscle mass and function observed after DOX exposure, which may lead to or aggravate cachexia, responsible for more than 20% of all cancer-related deaths.Os fármacos utilizados na quimioterapia como a doxorrubicina (DOX) são essenciais para o tratamento de vários tipos de cancro. No entanto, esta terapia tem vários efeitos secundários associados. A DOX pode potenciar a perda de massa muscular observada em pacientes com cancro, o que é particularmente preocupante em pacientes idosos. Assim, é necessário compreender os mecanismos responsáveis pela toxidade da DOX no músculo esquelético, de forma a identificar alvos terapêuticos e a aumentar as taxas de sobrevivência e qualidade de vida destes pacientes. Esta revisão discute os mediadores moleculares que poderão estar envolvidos na perda de massa muscular induzida pela DOX. Da análise realizada, a DOX parece promover a ativação da via da ubiquitina-proteassoma, ativação essa que pode ser intensificada pela elevação, induzida pela DOX, da atividade das vias da miostatina e do fator de necrose tumoral alfa, bem como pela presença de resistência à insulina. A DOX parece também induzir stress oxidativo e disfunção mitocondrial, o que poderá contribuir para a perda da massa muscular. Todos estes mecanismos parecem ser cruciais para impulsionar a perda de massa e de função muscular observadas após a exposição à DOX, o que poderá resultar ou agravar a caquexia, que é responsável por mais do que 20% de todas as mortes relacionadas com o cancro

    Optimization of gold core-mesoporous silica shell functionalization with TPGS and PEI for cancer therapy

    Get PDF
    Photothermal therapy (PTT) has captured the attention of different researchers around the world, since the application of NIR light responsive-nanomaterials has shown promising results in cancer therapy. Gold-core mesoporous silica shell (Au-MSS) nanoparticles allow the combination of gold mediated PTT with the drug delivery in order to improve their therapeutic potential. In this study, two different methodologies, electrostatic or chemical linkage, were explored to functionalize Au-MSS nanorods with TPGS and PEI. For that purpose, the TPGS and PEI were chemically coupled to each other or modified with 3-(triethoxysilyl)propyl isocyanate. The produced Au-MSS nanorods display a uniform morphology and a well-defined gold nucleus and silica shell. Further, the particles surface charge was dependent on the synthesis methodology. The particles modified by electrostatic interactions (Au-MSS/TPGS-PEI) were slightly negative (−16.9 and −5.1 mV) whereas the formulations produced by chemical linkage (Au-MSS/TPGS/PEI) resulted in positively charged nanoparticles (30.9 and 6.8 mV). The successful incorporation of the polymers was confirmed by Fourier Transformed Infrared spectroscopy and thermogravimetric analysis. Moreover, the Au-MSS functionalization did not affect the particles PTT capacity. However, the Au-MSS/TPGS/PEI nanorods displayed a decreased drug encapsulation efficiency. In vitro assays demonstrated the cytocompatibility of Au-MSS up to concentrations of 200 μg/mL, however the positively charged formulations only remained biocompatible until 100 and 125 μg/mL. Overall, the attained data confirm the successful modification of Au-MSS nanorods with TPGS and PEI as well as their applicability as PTT and drug delivery agents.info:eu-repo/semantics/publishedVersio

    Effects of the inoculation with soil microbiota onmaize grown in saline soils

    Get PDF
    food and energetic needs will thus increase dramatically, while conventional agriculture is, even actually, facing drastic reductions in production yields and/or severe increases in cost to compensate losses in productivity due to lower soil fertility
    corecore