Networking and participatory research promoting quality of life and well-being in Portuguese-speaking African countries

Spread across the planet each human being, individually or in community, aspires for well-being and quality of life, according to the ideal of each one. However, we all believe that there are always ways to live better. For many people the measurement of a better life translates into the guarantee of social rights, the right to basic services, good land, seed and sufficient nutritious food for their community members. The Mechanism to Facilitate the Participation of Universities in the Food and Nutrition Security Council of the Community of Portuguese Speaking Countries is a cooperative academic network fomented by the Community of Portuguese Speaking Countries (CPLP) with support from the Food and Agriculture Organization of the United Nations. This mechanism works with teaching, research and extension in the CPLP Food and Nutrition Security Strategy. The pillars of CPLP Strategy are the strengthening of the governance of public policies on Food and Nutrition Security at all levels of government, social protection based on guaranteeing access to food and family farming with a strategy to increase the availability of good quality food, promoting social and environmental sustainability. CPLP University Mechanism has provided training processes for technicianswho work in public policies for Food and Nutrition Security and has contributed to the strengthening of postgraduate programs in Portuguese-speaking African countries. As consequence, it has favored participatory research and mixed methods as a theoretical methodological approach. Therefore, it seeks to focus on the territories of Food and Nutrition Security practices to transform reality, as recommended by CPLP Strategy, however, with the autonomous assumptions of the collaborative network. This chapter presents how local researchers perceive the results of a process of inducing an academic network to transform the local reality and promote Food and Nutrition Security in the context of the CPLP.info:eu-repo/semantics/publishedVersio

The mismatch repair system protects against intergenerational GAA repeat instability in a Friedreich ataxia mouse model

Copyright @ 2012 Elsevier. The article can be accessed from the link below.This article has been made available through the Brunel Open Access Publishing Fund.Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disorder caused by a dynamic GAA repeat expansion mutation within intron 1 of the FXN gene. Studies of mouse models for other trinucleotide repeat (TNR) disorders have revealed an important role of mismatch repair (MMR) proteins in TNR instability. To explore the potential role of MMR proteins on intergenerational GAA repeat instability in FRDA, we have analyzed the transmission of unstable GAA repeat expansions from FXN transgenic mice which have been crossed with mice that are deficient for Msh2, Msh3, Msh6 or Pms2. We find in all cases that absence of parental MMR protein not only maintains transmission of GAA expansions and contractions, but also increases GAA repeat mutability (expansions and/or contractions) in the offspring. This indicates that Msh2, Msh3, Msh6 and Pms2 proteins are not the cause of intergenerational GAA expansions or contractions, but act in their canonical MMR capacity to protect against GAA repeat instability. We further identified differential modes of action for the four MMR proteins. Thus, Msh2 and Msh3 protect against GAA repeat contractions, while Msh6 protects against both GAA repeat expansions and contractions, and Pms2 protects against GAA repeat expansions and also promotes contractions. Furthermore, we detected enhanced occupancy of Msh2 and Msh3 proteins downstream of the FXN expanded GAA repeat, suggesting a model in which Msh2/3 dimers are recruited to this region to repair mismatches that would otherwise produce intergenerational GAA contractions. These findings reveal substantial differences in the intergenerational dynamics of expanded GAA repeat sequences compared with expanded CAG/CTG repeats, where Msh2 and Msh3 are thought to actively promote repeat expansions.This study is funded under European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement number 242193/EFACTS. This article is made available through the Brunel Open Access Publishing Fund

The Friedreich ataxia GAA repeat expansion mutation induces comparable epigenetic changes in human and transgenic mouse brain and heart tissues

Friedreich ataxia (FRDA) is caused by a homozygous GAA repeat expansion mutation within intron 1 of the FXN gene, leading to reduced expression of frataxin protein. Evidence suggests that the mutation may induce epigenetic changes and heterochromatin formation, thereby impeding gene transcription. In particular, studies using FRDA patient blood and lymphoblastoid cell lines have detected increased DNA methylation of specific CpG sites upstream of the GAA repeat and histone modifications in regions flanking the GAA repeat. In this report we show that such epigenetic changes are also present in FRDA patient brain, cerebellum and heart tissues, the primary affected systems of the disorder. Bisulfite sequence analysis of the FXN flanking GAA regions reveals a shift in the FRDA DNA methylation profile, with upstream CpG sites becoming consistently hypermethylated and downstream CpG sites becoming consistently hypomethylated. We also identify differential DNA methylation at three specific CpG sites within the FXN promoter and one CpG site within exon 1. Furthermore, we show by chromatin immunoprecipitation (ChIP) analysis that there is overall decreased histone H3K9 acetylation together with increased H3K9 methylation of FRDA brain tissue. Further studies of brain, cerebellum and heart tissues from our GAA repeat expansion-containing FRDA YAC transgenic mice reveal comparable epigenetic changes to those detected in FRDA patient tissue. We have thus developed a mouse model that will be a valuable resource for future therapeutic studies targeting epigenetic modifications of the FXN gene to increase frataxin expression

Academics engaging in knowledge transfer and co-creation: push causation and pull effectuation?

Although academics are increasingly engaging with businesses, some fundamental aspects of this phenomenon (i.e., their motivations, decision-making approaches, and the interplay between the two) remain understudied. We therefore conducted a qualitative inductive study comprising 68 interviews with academics who had engaged in two forms of activities—knowledge transfer and co-creation. Whereas the entrepreneurship literature offers a resource-based argument, we made an original contribution to the literature by introducing an engagement-based argument in order to offer a more accurate prediction of the motivations and decision-making approaches of academics engaged in knowledge transfer and co-creation activities. We found that when the resource- and engagement-based arguments offer different predictions of the interplay between the motivations and decision-making approaches adopted, the cognitive proximity between academics and business researchers, which reflects whether the partners are from the same/different disciplines, resolves the puzzle. We captured these situational contingencies by developing six propositions that indicate how the engagement- and resource-based arguments jointly offer a more comprehensive explanation of the interplay. We discuss the implications of our findings with regard to how universities could offer customized training, rewards, and support structures based on the four types of interplay between the motivation and decision-making approaches

Academics engaging in knowledge transfer and co-creation : Push causation and pull effectuation?

Although academics are increasingly engaging with businesses, some fundamental aspects of this phenomenon (i.e., their motivations, decision-making approaches, and the interplay between the two) remain understudied. We therefore conducted a qualitative inductive study comprising 68 interviews with academics who had engaged in two forms of activities—knowledge transfer and co-creation. Whereas the entrepreneurship literature offers a resource-based argument, we made an original contribution to the literature by introducing an engagement-based argument in order to offer a more accurate prediction of the motivations and decision-making approaches of academics engaged in knowledge transfer and co-creation activities. We found that when the resource- and engagement-based arguments offer different predictions of the interplay between the motivations and decision-making approaches adopted, the cognitive proximity between academics and business researchers, which reflects whether the partners are from the same/different disciplines, resolves the puzzle. We captured these situational contingencies by developing six propositions that indicate how the engagement- and resource-based arguments jointly offer a more comprehensive explanation of the interplay. We discuss the implications of our findings with regard to how universities could offer customized training, rewards, and support structures based on the four types of interplay between the motivation and decision-making approaches.© 2022 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).fi=vertaisarvioitu|en=peerReviewed

Pms2 suppresses large expansions of the (GAA·TTC)n sequence in neuronal tissues

Copyright @ 2012 Bourn et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Expanded trinucleotide repeat sequences are the cause of several inherited neurodegenerative diseases. Disease pathogenesis is correlated with several features of somatic instability of these sequences, including further large expansions in postmitotic tissues. The presence of somatic expansions in postmitotic tissues is consistent with DNA repair being a major determinant of somatic instability. Indeed, proteins in the mismatch repair (MMR) pathway are required for instability of the expanded (CAG·CTG)(n) sequence, likely via recognition of intrastrand hairpins by MutSβ. It is not clear if or how MMR would affect instability of disease-causing expanded trinucleotide repeat sequences that adopt secondary structures other than hairpins, such as the triplex/R-loop forming (GAA·TTC)(n) sequence that causes Friedreich ataxia. We analyzed somatic instability in transgenic mice that carry an expanded (GAA·TTC)(n) sequence in the context of the human FXN locus and lack the individual MMR proteins Msh2, Msh6 or Pms2. The absence of Msh2 or Msh6 resulted in a dramatic reduction in somatic mutations, indicating that mammalian MMR promotes instability of the (GAA·TTC)(n) sequence via MutSα. The absence of Pms2 resulted in increased accumulation of large expansions in the nervous system (cerebellum, cerebrum, and dorsal root ganglia) but not in non-neuronal tissues (heart and kidney), without affecting the prevalence of contractions. Pms2 suppressed large expansions specifically in tissues showing MutSα-dependent somatic instability, suggesting that they may act on the same lesion or structure associated with the expanded (GAA·TTC)(n) sequence. We conclude that Pms2 specifically suppresses large expansions of a pathogenic trinucleotide repeat sequence in neuronal tissues, possibly acting independently of the canonical MMR pathway.IDB was supported by a postdoctoral fellowship from the National Ataxia Foundation. RMP was supported by Ataxia UK. SA was supported by The Wellcome Trust. This research was made possible by grants from the National Institutes of Health (NIH/NINDS) and the Muscular Dystrophy Association to S.I.B

Advanced Maternal Age: Adverse Outcomes of Pregnancy, A Meta-Analysis

INTRODUCTION: The risks of pregnancy in women of advanced maternal age are not consensual amongst studies. The aim of this metaanalysis was to determine whether women of advanced maternal age (≥ 35 years old) had worse obstetrical and perinatal outcomes than non- advanced maternal age women (20 - 34 years old) in singleton, naturally-conceived pregnancies. MATERIAL AND METHODS: We searched PubMed/ MEDLINE, IndexRMP and the Cochrane Database of Systematic Reviews. Ten studies were included according to the following criteria: population of > 1000 nulliparous and/or multiparous women with singleton gestations who did not undergo any type of infertility treatment. Using Review Manager v. 5.3, two meta-analysis were performed: one comparing the outcomes of 20 - 34-year-old vs 35 - 40-year-old women, and another comparing the outcomes of 35 - 40-year-old women vs > 40-year-old women. RESULTS: Women aged 35 - 40 years old were more likely to have > 12 years of education than 20 - 34 years old and > 40 years old women. Advanced maternal age women (35 - 40 and > 40 years old) were more likely to be overweight and having gestational diabetes and gestational hypertension. They were also more likely to undergo induced labour and elective caesarean deliveries. Furthermore, they had worse perinatal outcomes such as preterm delivery, low birthweight babies, higher rates of Neonatal Intensive Care Unit admission and worse Apgar scores. Advanced maternal age women had higher rates of perinatal mortality and stillbirth. DISCUSSION: Most authors present similar results to our study. Although the majority of adverse outcomes can be explained through the physio-pathological changes regarding the female reproductive apparatus that come with aging and its inherent comorbidities, according to the existing literature advanced maternal age can be an independent risk factor per se. In older pregnant women without comorbidities such as gestational hypertension or diabetes there are still worse obstetric and perinatal outcomes, which indicate that advanced maternal age is an independent strong risk factor alone. CONCLUSION: Advanced maternal age women are at a higher risk of adverse obstetrical and perinatal outcomes. In both comparisons, worse outcomes were more prevalent in the older group, suggesting that poorer outcomes are more prevalent with increasing age.info:eu-repo/semantics/publishedVersio

Location of the dicyclohexylcarbodiimide-reactive glutamate residue in the bovine heart mitochondrial porin.

The mitochondrial porin or VDAC (Voltage-Dependent Anion Channel), the pore-forming structure responsible for the high permeability of the outer mitochondrial membrane, was found to be one of only three mitochondrial proteins bound by [14C]dicyclohexylcarbodiimide (DCCD) at low dosages (1.5 nmol/mg of mitochondrial porin) (De Pinto, V., Tommasino, M., Benz, R., and Palmieri, F. (1985) Biochim. Biophys. Acta 813, 230-242). Treatment of intact mitochondria with DCCD results in the inhibition of their ability to binding hexokinase (Nakashima, R. A., Mangan, P. S., Colombini, M., and Pedersen, P. L. (1986) Biochemistry 25, 1015-1021). In the present study, mitochondrial porin was purified from [14C]DCCD-labeled mitochondria. The purified labeled porin was treated with the cleavage reagent CNBr and with the endoproteases trypsin and V8 from Staphylococcus aureus and blotted to polyvinylidene difluoride membrane. The transferred peptides were detected with Coomassie Blue dye, excised, and sequenced. The sequences of several labeled and unlabeled peptides were obtained and then overlapped. The region containing the [14C]DCCD radioactivity was limited to 50 amino acid residues and completely sequenced. Covalently incorporated [14C]DCCD was exclusively released at the position corresponding to glutamate 72. The DCCD-reactive residue is located in the 4th of 16 predicted transmembrane amphipathic beta-strands. When the sequence surrounding the DCCD site was compared to those surrounding the DCCD-reactive residue of other membrane proteins, no homology was apparent

Transmission fiber chromatic dispersion dependence on temperature: implications on 40 Gb/s performance

In this letter we will evaluate the performance degradation of a 40 km high-speed (40 Gb/s) optical System, induced by optical fiber variations of the chromatic dispersion induced by temperature changes. The chromatic dispersion temperature sensitivity will be estimated based on the signal quality parameters