Avaliação de grupo de educação nutricional para mulheres com excesso de peso

Dissertação (mestrado)—Universidade de Brasília, Instituto de Psicologia, Programa de Pós-Graduação em Processos de Desenvolvimento Humano e Saúde, 2012.O crescimento do excesso de peso na população aponta para a necessidade de criação de estratégias efetivas para a incorporação de hábitos alimentares saudáveis. Nesse sentido, propõem-se abordagens educativas pautadas no modelo biopsicossocial de atenção à saúde, que permitem o enfoque dos problemas alimentares em sua complexidade e envolvem os pacientes como sujeitos ativos do processo. Dentre eles, destaca-se o modelo cognitivo, que vem se mostrando efetivo em programas de mudanças de hábitos de vida. Assim, o objetivo geral desse projeto foi propor e avaliar um programa de educação nutricional baseado no modelo cognitivo como estratégia para adoção de hábitos alimentares saudáveis e redução do peso e do risco cardiovascular em mulheres com sobrepeso e obesidade. Para tanto, realizou-se um estudo quase-experimental com metodologia quali-quantitativa, do qual participaram 39 mulheres adultas com excesso de peso atendidas na rede pública de saúde do Distrito Federal, que foram alocadas em dois grupos: um de atendimento coletivo (Grupo Experimental n=23) e outro individual (Grupo Controle n=16). O Grupo Experimental participou do programa de educação nutricional coletivo composto por 13 encontros semanais pautado no modelo cognitivo e o Grupo Controle recebeu acompanhamento nutricional individual tradicional, conforme os procedimentos já padronizados pelo serviço onde o estudo foi realizado. A pesquisa teve duração de três meses. Dados antropométricos, bioquímicos e de pressão arterial foram comparados entre os grupos e dificuldades referentes ao processo de emagrecimento foram investigadas através de uma entrevista aberta. Ao final, verificou-se que a amostra estudada apresentou redução no consumo energético, de carboidratos e fibras, e concomitante aumento na ingestão proteica. O Grupo Controle apresentou uma perda média de peso de 900g e redução média na circunferência abdominal de 1,15cm, enquanto que no Grupo Experimental as participantes perderam uma média de 2,03kg e 3,48cm de circunferência abdominal. A comparação entre os grupos apresentou valores não significativos (p=0,1827 e p=0,0603, respectivamente). Os dados bioquímicos (glicose em jejum e lipídios séricos) e de pressão arterial, também não diferiram significativamente entre os grupos ao final do programa. As principais dificuldades relatadas em relação ao processo de emagrecimento estavam relacionadas ao planejamento alimentar, velocidade de realização das refeições, alimentação noturna e fracionamento da dieta, bem como à dificuldade de manter a dieta em situações não rotineiras e compromissos sociais e lidar com as tentações alimentares. Os principais fatores citados como facilitadores do emagrecimento foram: a realização de dietas não radicais e viáveis, flexibilidade de cognições dicotômicas, dieta variada, estabelecimento de metas realistas, apoio social, possibilidade de troca de experiências e educação nutricional. Na perspectiva das participantes, o programa foi avaliado como relevante, especialmente no que diz respeito à tomada de consciência para a mudança. Conclui-se que apesar da comparação das variáveis objetivas entre os grupos não ter se apresentado significativa, a análise das entrevistas mostrou que o programa auxiliou em mudanças na alimentação no aspecto qualitativo e quantitativo, bem como atingiu seu objetivo de conscientizar as participantes da importância de mudanças mais amplas no estilo de vida para perda de peso e manutenção da saúde. _____________________________________________________________________________ ABSTRACTThe increase of overweight in population indicates a need to develop strategies that are effective in incorporating healthy eating habits. Thus, it is proposed educational strategies grounded in a biopsychosocial approach on health attention, addressing diet issues in their entirety by involving patients as active member in the process. Within this approach, the cognitive model is highlighted as effective in programs that work towards changes in lifestyle. Hence, the overall goal of this project was to propose and evaluate a nutritional education program based on the cognitive model as a strategy to adopt healthy eating habits, as well as weight and cardiovascular risk reduction in women that are overweight and obese. For this purpose, we conducted a quasi-experimental study with qualitative and quantitative methodology, which involved 39 overweight adult women care in public health in the Federal District, which were allocated into two groups: a attendee (Experimental n=23) and an individual (Control n=16). The experimental group participated in a collective nutritional education program consisting of 13 weekly meetings and the control group received individual nutritional counseling, as standardized procedures of the service where the study was conducted. The study lasted during three months. Anthropometric, biochemical and blood pressure were compared between the groups and the difficulties regarding the weight loss process were investigated through an open interview. In the end, it was found that the sample studied had reduced energy consumption, carbohydrate and fiber, and concomitant increase in protein intake. The control group showed a mean weight loss of 900g and an average reduction in waist circumference of 1.15 cm, while the experimental group participants lost an average of 2.03 kg and 3.48 cm in waist circumference. The comparison between groups showed no significant values (p = 0.1827 and p = 0.0603, respectively). Biochemical data (fasting glucose and serum lipids) and blood pressure did not differ significantly between groups at the end of the program. The main difficulties reported by participants in regards to weight loss were related to diet plans, time consumed in meals, night treats and meal frequency, as well as the difficulty of sticking with the diet in non-routine situations and social commitments and dealing with temptations food. The main facilitating factors of weight loss were: non radical diets and feasible nourishments, demystification of forbidden foods, diets with food substitution possibilities, setting realistic goals, social support, possibility of exchanging experiences amongst patients and nutritional education. From the participants perspective, the program was evaluated as relevant, especially regarding awareness towards change. We conclude that despite the comparison between groups being non significantly based on objective criteria, the analysis of the interviews showed that the program helped dietary changes in qualitative and quantitative aspects, and reached its goal to educate participants as to the importance of broader changes in lifestyle in order to loss weight and maintain health

Combined therapy with m-TOR-dependent and -independent autophagy inducers causes neurotoxicity in a mouse model of Machado-Joseph disease

A major pathological hallmark in several neurodegenerative disorders, like polyglutamine disorders (polyQ), including Machado-Joseph disease (MJD), is the formation of protein aggregates. MJD is caused by a CAG repeat expansion in the ATXN3 gene, resulting in an abnormal protein, which is prone to misfolding and forms cytoplasmic and nuclear aggregates within neurons, ultimately inducing neurodegeneration. Treatment of proteinopathies with drugs that up-regulate autophagy has shown promising results in models of polyQ diseases. Temsirolimus (CCI-779) inhibits the mammalian target of rapamycin (m-TOR), while lithium chloride (LiCl) acts by inhibiting inositol monophosphatase, both being able to induce autophagy. We have previously shown that chronic treatment with LiCl (10.4 mg/kg) had limited effects in a transgenic MJD mouse model. Also, others have shown that CCI-779 had mild positive effects in a different mouse model of the disease. It has been suggested that the combination of mTOR-dependent and -independent autophagy inducers could be a more effective therapeutic approach. To further explore this avenue toward therapy, we treated CMVMJD135 transgenic mice with a conjugation of CCI-779 and LiCl, both at concentrations known to induce autophagy and not to be toxic. Surprisingly, this combined treatment proved to be deleterious to both wild-type (wt) and transgenic animals, failing to rescue their neurological symptoms and actually exerting neurotoxic effects. These results highlight the possible dangers of manipulating autophagy in the nervous system and suggest that a better understanding of the potential disruption in the autophagy pathway in MJD is required before successful long-term autophagy modulating therapies can be developed.Fundação para a Ciência e Tecnologia through the projects [FEDER/FCT, POCI/SAU-MMO/60412/2004], [PTDC/SAU-GMG/64076/2006]. This work was supported by Fundação para a Ciência e Tecnologi

Processo de obtenção de membrana polimérica, membrana polimérica e uso da membrana polimérica

Universidade Federal do Rio Grande do SulQuímicaDepositad

Fortificações da foz do Tejo

Dissertação de mestrado em Arquitectura, Universidade Lusíada de Lisboa, 2014Exame público realizado em 9 de Maio de 2014Hoje é possível observar, ao longo da margem Norte do rio Tejo junto à foz, construções centenárias de caráter militar implantadas em locais estratégicos e sobranceiros à linha de água, como guaritas mirantes do curso das águas ou alguns barcos que por ali passam. Sobre a decisão de alguém as ter erguido nesses locais, levantam-se diversas questões: - Terão sido erguidas na mesma época? E por que razão ou por quem? - Tendo elas diferentes dimensões, quererão refletir uma hierarquia de funcionamento ou uma necessidade de atividade militar? E como é que funcionavam? - E porque é que é possível observar estas construções apenas entre Caxias e o Cabo da Roca? Seria a defesa diferente, nas zonas mais próximas de Lisboa? Neste trabalho, que ora se inicia pretende-se responder a estas questões, vivenciando os edifícios in loco, observando as relações de localização que estabelecem entre si e analisando cartografia ancestral que os incluía, tanto em descrição como em representação. Ao longo da investigação foram surgindo documentos de diversas épocas, de uma forma geral cartográficos, que evidenciavam um plano estratégico de defesa do Porto de Lisboa. Estas ideias, remontam ao reinado de D. João I com implementação efetiva um século mais tarde com D. João II (e narrada por Garcia de Resende). Estes planos consistiam numa primeira fase em dotar a foz do rio com uma barreira armada composta por dois baluartes entre Belém e o actual local de Porto Brandão, implantados onde o términus do rio é mais estreito. A defesa foi sendo desenvolvida e o plano acabou por ser bem mais ambicioso que apenas a construção destes dois baluartes. Este passou a incluir o reforço de posições em toda a margem Norte e Sul do rio, com novas barreiras fluviais, pontos de vigia e controlo da área atlântica. O desenho dos fortes está directamente associado com o início da utilização da pólvora e, na medida em que a artilharia evoluiu, deixaram de desempenhar o seu papel militar e a funcionalidade para a qual tinham sido edificadas

The Notch Ligand Delta-Like 4 Regulates Multiple Stages of Early Hemato-Vascular Development

Background: In mouse embryos, homozygous or heterozygous deletions of the gene encoding the Notch ligand Dll4 result in early embryonic death due to major defects in endothelial remodeling in the yolk sac and embryo. Considering the close developmental relationship between endothelial and hematopoietic cell lineages, which share a common mesodermderived precursor, the hemangioblast, and many key regulatory molecules, we investigated whether Dll4 is also involved in the regulation of early embryonic hematopoiesis. Methodology/Principal Findings: Using Embryoid Bodies (EBs) derived from embryonic stem cells harboring hetero- or homozygous Dll4 deletions, we observed that EBs from both genotypes exhibit an abnormal endothelial remodeling in the vascular sprouts that arise late during EB differentiation, indicating that this in vitro system recapitulates the angiogenic phenotype of Dll4 mutant embryos. However, analysis of EB development at early time points revealed that the absence of Dll4 delays the emergence of mesoderm and severely reduces the number of blast-colony forming cells (BL-CFCs), the in vitro counterpart of the hemangioblast, and of endothelial cells. Analysis of colony forming units (CFU) in EBs and yolk sacs from Dll4 +/2 and Dll4 2/2 embryos, showed that primitive erythropoiesis is specifically affected by Dll4 insufficiency. In Dll4 mutant EBs, smooth muscle cells (SMCs) were seemingly unaffected and cardiomyocyte differentiation was increased, indicating that SMC specification is Dll4-independent while a normal dose of this Notch ligand is essential for th

Profiling microglia in a mouse model of Machado-Joseph disease

Microglia have been increasingly implicated in neurodegenerative diseases (NDs), and specific disease associated microglia (DAM) profiles have been defined for several of these NDs. Yet, the microglial profile in Machado–Joseph disease (MJD) remains unexplored. Here, we characterized the profile of microglia in the CMVMJD135 mouse model of MJD. This characterization was performed using primary microglial cultures and microglial cells obtained from disease-relevant brain regions of neonatal and adult CMVMJD135 mice, respectively. Machine learning models were implemented to identify potential clusters of microglia based on their morphological features, and an RNA-sequencing analysis was performed to identify molecular perturbations and potential therapeutic targets. Our findings reveal morphological alterations that point to an increased activation state of microglia in CMVMJD135 mice and a disease-specific transcriptional profile of MJD microglia, encompassing a total of 101 differentially expressed genes, with enrichment in molecular pathways related to oxidative stress, immune response, cell proliferation, cell death, and lipid metabolism. Overall, these results allowed us to define the cellular and molecular profile of MJD-associated microglia and to identify genes and pathways that might represent potential therapeutic targets for this disorder.This work was supported by Fundação para a Ciência e a Tecnologia (FCT) (PTDC/NEUNMC/3648/2014) and COMPETE-FEDER (POCI-01-0145-FEDER-016818). It was also supported by Portuguese funds through FCT in the framework of the Project POCI-01-0145-FEDER-031987 (PTDC/MED-OUT/31987/2017). A.B.C. was supported by a doctoral fellowship from FCT (PD/BD/ 127828/2016). S.P.N. was also supported by FCT (PD/BD/114120/2015). Work in the JBR laboratory was financed by FEDER—Fundo Europeu de Desenvolvimento Regional funds through the COMPETE 2020—Operational Programme for Competitiveness and Internationalization (POCI), Portugal 2020, and by Portuguese funds through FCT in the framework of the Project POCI-01-0145- FEDER030647 (PTDC/MED-NEU/31318/2017). This work was funded by ICVS Scientific Microscopy Platform, member of the national infrastructure PPBI (Portuguese Platform of Bioimaging) (PPBIPOCI-01-0145-FEDER-022122), and by National funds, through FCT—project UIDB/50026/2020 and UIDP/50026/2020

Genetic ablation of inositol 1,4,5-Trisphosphate receptor type 2 (IP3R2) fails to modify disease progression in a mouse model of Spinocerebellar Ataxia type 3

Spinocerebellar ataxia type 3 (SCA3) is a rare neurodegenerative disease caused by an abnormal polyglutamine expansion within the ataxin-3 protein (ATXN3). This leads to neurodegeneration of specific brain and spinal cord regions, resulting in a progressive loss of motor function. Despite neuronal death, non-neuronal cells, including astrocytes, are also involved in SCA3 pathogenesis. Astrogliosis is a common pathological feature in SCA3 patients and animal models of the disease. However, the contribution of astrocytes to SCA3 is not clearly defined. Inositol 1,4,5-trisphosphate receptor type 2 (IP3R2) is the predominant IP3R in mediating astrocyte somatic calcium signals, and genetically ablation of IP3R2 has been widely used to study astrocyte function. Here, we aimed to investigate the relevance of IP3R2 in the onset and progression of SCA3. For this, we tested whether IP3R2 depletion and the consecutive suppression of global astrocytic calcium signalling would lead to marked changes in the behavioral phenotype of a SCA3 mouse model, the CMVMJD135 transgenic line. This was achieved by crossing IP3R2 null mice with the CMVMJD135 mouse model and performing a longitudinal behavioral characterization of these mice using well-established motor-related function tests. Our results demonstrate that IP3R2 deletion in astrocytes does not modify SCA3 progression.This work has been funded by National funds, through the Foundation for Science and Technology (FCT)—project UIDB/50026/2020 and UIDP/50026/2020, PTDC/NEUNMC/3648/2014 and COMPETE-FEDER (POCI-01-0145-FEDER-016818); fellowships to DCG (2021.08121.BD), DMF (SFRH/BD/147947/2019), JSC (SFRH/BD/140624/2018), ANC (SFRH/BPD/118779/2016), AVF (UMINHO/BIL-CNCG/2022/11), SGG (SFRH/BD/101298/2014), and JFV (2020.05109.BD); FCT Scientific Employment Stimulus (CEEC)—Individual Call position to SDS (CEECIND/00685/2020); grants from the Bial Foundation (037/18) and “the la Caixa” Foundation (LCF/PR/HR21/52410024) to JFO; and by the projects NORTE-01-0145-FEDER-000013 and NORTE-01-0145-FEDER-000023, supported by the Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF). It was also supported by grants from the ICVS Scientific Microscopy Platform, a member of the national infrastructure PPBI—Portuguese Platform of Bioimaging (PPBI-POCI-01-0145-FEDER-022122 and national funds through the Foundation for Science and Technology (FCT)

Differential effects of carbon-based and iron-based conductive materials in anaerobic butyrate-degrading enrichments

Introduction Conductive materials (CM) accelerate methane production (MP), probably by promoting more efficient interactions between bacteria and methanogens. This work investigates the effects of activated carbon (AC) and magnetite (Mag) in microbial enrichments degrading butyrate. Three different butyrate-degrading enrichments were developed: 1) without CM, 2) with AC, or 3) with Mag. It was also investigated if the effect of CM persisted when CM-adapted enrichments were transferred to new medium without CM, and if CM affected the activity of stable enrichments without previous contact with CM. Methodology Enrichment series were initiated with granular anaerobic sludge as inoculum, butyrate (10 mmol/L) as substrate, and CM (0.5 g/L AC or 0.5 g/L Mag), or without CM, and incubated at 37 °C, under strict anaerobic conditions. The following parameters were monitored: methane by gas chromatography; butyrate and acetate by high performance liquid chromatography; oxidation-reduction potential; pH and conductivity. RNA was extracted and taxonomic composition of the microbial communities was obtained by 16S rRNA gene sequencing. Results During the first incubations, AC-enrichment consumed hydrogen derived from butyrate degradation within 4 days, which was much faster than the enrichments with Mag and without CM, which presented lag phases (LP), preceding MP, longer than 11 and 7 days, respectively. Thus, Mag probably inhibited butyrate-degrading bacteria and/or hydrogenotrophic methanogens. Conversely, after the lag phase, Mag-enrichment was the fastest converting acetate to methane (3 times faster than in AC-enrichment), suggesting a stimulatory effect of Mag towards acetoclastic methanogens. Nevertheless, once the enrichments were adapted to the growth conditions, more efficient butyrate conversion was observed by all enrichments, with lag phases lower than 4 days, even in the control-enrichment. No significant changes on butyrate degradation were observed when highly adapted CM-enrichments were transferred to fresh medium without CM. On the other hand, when active enrichments (without previous contact with CM), were incubated with AC, it became slightly faster (0.7 times shorter LP), and with Mag were greatly inhibited (12 times longer LP). Syntrophomonas spp. represented 60 to 80 % of the total bacterial communities in all enrichments. Hydrogenotrophs were more abundant in AC-enrichment (78 % of Methanomicrobiales) and Mag-enrichment was highly enriched in acetoclastic methanogens (43 % of microorganisms assigned to Methanosaeta and Methanosarcina). Conclusions The presence of CM affects the performance of butyrate-degrading communities, with AC accelerating particularly butyrate conversion to methane (via H2/CO2) and acetate, and Mag inhibiting that first step but stimulating acetate conversion to methane.info:eu-repo/semantics/publishedVersio

Selective impact of Tau loss on nociceptive primary afferents and pain sensation

Tau protein hyperphosphorylation and consequent malfunction are hallmarks of Alzheimer's disease pathology; importantly, pain perception is diminished in these patients. In physiological conditions, Tau contributes to cytoskeletal dynamics and in this way, influences a number of cellular mechanisms including axonal trafficking, myelination and synaptic plasticity, processes that are also implicated in pain perception. However, there is no in vivo evidence clarifying the role of Tau in nociception. Thus, we tested Tau-null (Tau-/-) and Tau+/+ mice for acute thermal pain (Hargreaves' test), acute and tonic inflammatory pain (formalin test) and mechanical allodynia (Von Frey test). We report that Tau-/- animals presented a decreased response to acute noxious stimuli when compared to Tau+/+ while their pain-related behavior is augmented under tonic painful stimuli. This increased reactivity to tonic pain was accompanied by enhanced formalin-evoked c-fos staining of second order nociceptive neurons at Tau-null dorsal horn. In addition, we analyzed the primary afferents conveying nociceptive signals, estimating sciatic nerve fiber density, myelination and nerve conduction. Ultrastructural analysis revealed a decreased C-fiber density in the sciatic nerve of Tau-null mice and a hypomyelination of myelinated fibers (Ad-fibers) - also confirmed by western blot analysis - followed by altered conduction properties of Tau-null sciatic nerves. To our knowledge, this is the first in vivo study that demonstrates that Tau depletion negatively affects the main systems conveying nociceptive information to the CNS, adding to our knowledge about Tau function(s) that might also be relevant for understanding peripheral neurological deficits in different Tauopathies.We would like to thank Drs Joao Relvas, Joana Paes de Faria Monteiro and Nuno Dias for their comments in this work. Many thanks to Dr Joao Relvas for the MBP antibody. The work was supported by grants "SFRH/BPD/80118/2011", "PTDC/SAU-NMC/113934/2009" funded by FCT - Portuguese Foundation for Science and Technology and project DoIT - Desenvolvimento e Operacionalizacao da Investigacao de Translacao (No. do projeto 13853), funded by Fund Europeu de Desenvolvimento Regional (FEDER) through the Programa Operacional Fatores de Competitividade (POFC). Author's contributions: experimental design - IS, HA, VP, AA, and NS; performed research - IS, HA, VP, AL, SL, SS, SP, AC, FPR, and RF; data analyses - IS, HA, AL, VP, SC, and FPR; and manuscript preparation - IS, HA, VP, and NS

Preclinical assessment of mesenchymal-stem-cell-based therapies in spinocerebellar ataxia type 3

The low regeneration potential of the central nervous system (CNS) represents a challenge for the development of new therapeutic strategies for neurodegenerative diseases, including spinocerebellar ataxias. Spinocerebellar ataxia type 3 (SCA3)—or Machado–Joseph disease (MJD)—is the most common dominant ataxia, being mainly characterized by motor deficits; however, SCA3/MJD has a complex and heterogeneous pathophysiology, involving many CNS brain regions, contributing to the lack of effective therapies. Mesenchymal stem cells (MSCs) have been proposed as a potential therapeutic tool for CNS disorders. Beyond their differentiation potential, MSCs secrete a broad range of neuroregulatory factors that can promote relevant neuroprotective and immunomodulatory actions in different pathophysiological contexts. The objective of this work was to study the effects of (1) human MSC transplantation and (2) human MSC secretome (CM) administration on disease progression in vivo, using the CMVMJD135 mouse model of SCA3/MJD. Our results showed that a single CM administration was more beneficial than MSC transplantation—particularly in the cerebellum and basal ganglia—while no motor improvement was observed when these cell-based therapeutic approaches were applied in the spinal cord. However, the effects observed were mild and transient, suggesting that continuous or repeated administration would be needed, which should be further tested.This research was funded by the National Ataxia Foundation (NAF) and by Portuguese national funds, through the Foundation for Science and Technology (FCT)—projects UIDB/50026/2020, UIDP/50026/2020, POCI-01-0145-FEDER-029206, and through the Santa Casa Neuroscience Awards (Santa Casa da Misericórdia Lisboa)—project MC-04/17. Additionally, this project was funded by the ICVS Scientific Microscopy Platform, a member of the national infrastructure PPBI—Portuguese Platform of Bioimaging (PPBI-POCI-01-0145-FEDER-022122). S.C.S. received an individual fellowship within the project TUBITAK/0007/2014. The FCT funded individual fellowships to J.S C., A.N.-C., B.M.- P., F.G.T., R.L., S.M., N.A.S., C.S.-C., and S.D.-S. (SFRH/BD/140624/2018, SFRH/BPD/118779/2016, SFRH/BD/120124/2016, SFRH/BPD/118408/2016, PD/BDE/127836/2016, CEECIND/01902/2017, CEECIND/04794/2017, CEECIND/03887/2017, and CEECIND/00685/2020)