Obesity Rates in OECD Countries: An International Perspective

Food Consumption/Nutrition/Food Safety,

Obesity Rates in OECD Countries: An International Perspective

Obesity is a growing concern. New World Health Organization (WHO) figures indicate that obesity is spreading around the world as a "global epidemic." According to the WHO, there are more people suffering overweight related problems than malnutrition. Globally there are more than 1 billion adults who are overweight and at least 300 million of them are clinically obese, while 800 million suffer malnutrition (WHO 2004). The body mass index (BMI) is a common and accepted measure to report obesity rates (see WHO 1997). BMI is measured as weight in kilograms divided by height in meters squared. Recommended BMI levels are generally between a numerical value of 20 and 25. An individual with a BMI between 25 and 30 is considered overweight, while an individual with a BMI above 30 is considered obese. Individuals with BMIs below 20 are considered thin.Food Consumption/Nutrition/Food Safety,

ANALYZING CROSS-COUNTRY DIFFERENCES IN OBESITY RATES: SOME POLICY IMPLICATIONS

Replaced with revised version of paper 07/30/04.Health Economics and Policy,

A repeat-primed PCR assay for pentanucleotide repeat alleles in spinocerebellar ataxia type 37

Spinocerebellar ataxia 37 (SCA37) is caused by an (ATTTC)n insertion in a polymorphic ATTTT repeat in the non-coding region of DAB1. The non-pathogenic alleles have a configuration [(ATTTT)7-400], whereas pathogenic alleles have a complex structure of [(ATTTT)60-79(ATTTC)31-75(ATTTT)58-90]. Molecular diagnosis of SCA37 is laborious because about 7% of the pentanucleotide repeat alleles in DAB1 are larger than 30 units and, thus, fail to amplify with standard PCR conditions, resulting in apparently homoallelism or in complete lack of PCR amplification in several cases. The molecular test currently available requires long-range PCR and sequencing analysis for the detection and characterization of these large alleles. We developed a simple assay capable of rapidly detecting the presence or absence of large pentanucleotide repeat sizes. This assay is based on repeat-primed PCR followed by high-throughput capillary electrophoresis. Combining the standard PCR with RP-PCR allows completion of the diagnosis in more than 80% of individuals, minimizing the number of samples that require long-range PCR followed by Sanger sequencing analysis. This assay meets many of the requirements for pre-screening of large cohorts of affected individuals.This work was funded by Fundo Europeu de Desenvolvimento Regional-FEDER funds through the COMPETE 2020—Operational Programme for Competitiveness and Inter- nationalisation (POCI), Portugal 2020, and by funding from FCT— Fundação para a Ciência e a Tecnologia/Ministério da Ciência, Tec- nologia e Inovação, Portugal, in the framework of the project “Institute for Research and Innovation in Health Sciences” (POCI-01-0145- FEDER-007274); by Grant PTDC/SAU-GMG/098305/2008, from FCT, to I.S. J.R.L. was supported by scholarships from Grant PTDC/ GMG-SAU/098305/2008, FCT, PEst- C/SAU/LA0002/2013 and EMBO (ASTF494-2015). C.L.O. was supported by a scholarship from PEst-C/SAU/LA0002/2013. This work was also funded by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (FEDER), Portugal, that supports the Norte-01-0145-FEDER-000008—Porto Neurosciences and Neurologic Disease Research Initiative at I3S

Mutational mechanism for DAB1 (ATTTC) n insertion in SCA37: ATTTT repeat lengthening and nucleotide substitution

Dynamic mutations by microsatellite instability are the molecular basis of a growing number of neuromuscular and neurodegenerative diseases. Repetitive stretches in the human genome may drive pathogenicity, either by expansion above a given threshold, or by insertion of abnormal tracts in nonpathogenic polymorphic repetitive regions, as is the case in spinocerebellar ataxia type 37 (SCA37). We have recently established that this neurodegenerative disease is caused by an (ATTTC)n insertion within an (ATTTT)n in a noncoding region of DAB1. We now investigated the mutational mechanism that originated the (ATTTC)n insertion within an ancestral (ATTTT)n . Approximately 3% of nonpathogenic (ATTTT)n alleles are interspersed by AT-rich motifs, contrarily to mutant alleles that are composed of pure (ATTTT)n and (ATTTC)n stretches. Haplotype studies in unaffected chromosomes suggested that the primary mutational mechanism, leading to the (ATTTC)n insertion, was likely one or more T>C substitutions in an (ATTTT)n pure allele of approximately 200 repeats. Then, the (ATTTC)n expanded in size, originating a deleterious allele in DAB1 that leads to SCA37. This is likely the mutational mechanism in three similar (TTTCA)n insertions responsible for familial myoclonic epilepsy. Because (ATTTT)n tracts are frequent in the human genome, many loci could be at risk for this mutational process.We are grateful to the families and individuals who participated in this work. We thank Patricia Ribeiro for technical assistance. This study was financed by Fundo Europeu de Desenvolvimento Regional (FEDER), through the COMPETE 2020 Operational Pro- gram for Competitiveness and Internationalization (POCI) of Portugal 2020, and by the Fundacão para a Ciência e a Tecnologia (FCT) and Ministério da Ciência, Tecnologia e Ensino Superior (Portugal), in the framework of the project POCI-01-0145-FEDER-029255; (PTDC/MED-GEN/29255/2017) to I.S. J.R.L. and C.L.O. were sup- ported by scholarships from PEst-C/SAU/LA0002/2013. S.M. is funded by the project IF/00930/2013/ CP1184/CT0002 from FCT. This work was also funded by the Porto Neurosciences and Neurologic Disease Research Initiative at the Instituto de Investigação e Inovação em Saúde (Norte-01-0145-FEDER- 000008), supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTU- GAL 2020 Partnership Agreement with FEDER

A educação ambiental como política pública para gestão integrada dos recursos naturais: um estudo de caso do município de Paragominas no estado do Pará

Este artigo tem por objetivo analisar a educação ambiental como uma política pública implementada pelo município de Paragominas na gestão dos recursos naturais locais, como resposta à grave crise social, econômica, ecológica e cultural que aquela comunidade atravessou nas últimas décadas. Apesar de suas peculiaridades, esse município é um espaço geopolítico representativo da realidade ambiental e dos conflitos que o uso dos recursos naturais enseja na região amazônica. Sua resposta a essa crise tornou-se conhecida nacionalmente, merecedora de análise, que identificou e tipificou seus ciclos à luz das teorias sobre políticas públicas e da educação ambiental como campo de articulação entre o saber e a ética. Como resultado, são apresentados os ciclos pelos quais passaram essa política local e uma contribuição ao CONAMA (Conselho Nacional do Meio Ambiente) visando regulamentar programas de educação ambiental

Os sonhos são as janelas da aula: reflexões acadêmico-vivenciais

Este artigo discute realidades e possibilidades didáticas de uma aula, considerando a perspectiva da aprendizagem, ao contrário do que propunha a chamada didática tradicional, que enfatizava o ensino. O enfoque mais educativo já não comporta uma relação unidirecional de ensino-aprendizagem (o professor ensina, o aluno aprende, ou o que o professor ensina, o aluno aprende), o professor detém o discurso, a fala (principalmente), o aluno "engole" esse discurso (ouvindo, na maioria das vezes), professor é o que sabe e o aluno, o ignorante. É preciso, pois, haver integração entre o processo de ensino com o processo de aprendizagem. O processo de ensino deve estabelecer apenas exigências e expectativas que os alunos possam cumprir para poder realmente envolvê-los nesse processo e mobilizar as suas energias. Os conteúdos não podem mais ser repetidos os mesmos ao longo dos tempos. Torna-se necessária uma transformação didática, reflexiva, para que eles adquiram um significado atualizado com o tempo dos estudantes e da sociedade em que vivem. Também é preciso que haja um novo sistema e um novo contexto de trabalho para os docentes: não é mais possível admitir um trabalho isolado, exige-se o trabalho em grupo, envolvendo todos os estudantes, professores, técnicos e demais profissionais da escola.Palavras Chave: Didática - Ensino e Aprendizagem - Trabalho coletivoThe dreams are the windows of the class: experiential academic resolutionsThis paper discusses the realities and didactic possibilities of a class, considering the learning perspective, in contrast to what the traditional didactic used to propose, which emphasized the teaching. The most educational approach no longer has a one-way teaching-learning relationship (the teacher teaches, the student learns or what the teacher teaches, the student learns), the student "swallows" this speech (listening, most of the time), teacher is the one who knows and the student, the ignorant. So, it's necessary having integration between the teaching and learning processes. The teaching process should only establish requirements and expectations that students can fulfill to really engage them in this process and mobilize their energies. The contents can no longer be repeated over time. It's necessary a didactic and reflexive transformation, so that they acquire an updated meaning with the students time and the society in which they live. It is also necessary to have a new system and a new working context for teachers: it is no longer possible to admit an isolated work, group work is required, involving all the students, teachers, technicians and other school professionals.Keywords: Didacticism - Teaching and Learning - Collective work" " " "

S14. DNA methylation changes in GABAergic and glutamatergic markers in early schizophrenia.

Background: GABAergic and glutamatergic systems play an important role in the neurobiology of schizophrenia, and changes in their markers are reported in both postmortem human brain and in animal models. Recent studies have demonstrated that abnormalities in DNA methylation may underlie the alterations in various indicators of GABAergic and glutamatergic functions in schizophrenia. As our group previously found decreased NR2 protein plasma levels and downregulation of parvalbumin (PVALB) mRNA in first episode of psychosis (FEP) patients, we hypothesised that changes in DNA methylation may be responsible for these indicators of glutamatergic and GABAergic deficits in FEP patients. Methods: Blood samples were collected from patients in FEP (n = 35) after their first contact with the mental health assistance, siblings (n = 21) and population-based controls (n = 35). Bisulfite conversion and pyrosequencing were used to determine methylation levels in 4 CpG sites in promoter sequence of PVALB and 5 CpG sites at GRIN2B (gene which encodes NR2). Results: We found hypermethylation at a CpG site within the PVALB promoter sequence in patients and their siblings compared to population-based control group (p< 0.001) while overall hypomethylation was found in the 5 CpGs analysed within GRIN2B promoter sequence (p < 0.01). Discussion: Our PVALB findings are consistent with our previous studies showing that PVALB promoter methylation is elevated in schizophrenia and, additionally this is the first evidence showing changes in GRIN2B promoter methylation in psychosis. These results together suggest that these epigenetic findings may relate to the reduction of protein expression of indicators of glutamate and GABA systems seen in this disease

A pentanucleotide ATTTC repeat insertion in the non-coding region of DAB1, mapping to SCA37, causes spinocerebellar ataxia.

Advances in human genetics in recent years have largely been driven by next-generation sequencing (NGS); however, the discovery of disease-related gene mutations has been biased toward the exome because the large and very repetitive regions that characterize the non-coding genome remain difficult to reach by that technology. For autosomal-dominant spinocerebellar ataxias (SCAs), 28 genes have been identified, but only five SCAs originate from non-coding mutations. Over half of SCA-affected families, however, remain without a genetic diagnosis. We used genome-wide linkage analysis, NGS, and repeat analysis to identify an (ATTTC)n insertion in a polymorphic ATTTT repeat in DAB1 in chromosomal region 1p32.2 as the cause of autosomal-dominant SCA; this region has been previously linked to SCA37. The non-pathogenic and pathogenic alleles have the configurations [(ATTTT)7-400] and [(ATTTT)60-79(ATTTC)31-75(ATTTT)58-90], respectively. (ATTTC)n insertions are present on a distinct haplotype and show an inverse correlation between size and age of onset. In the DAB1-oriented strand, (ATTTC)n is located in 5' UTR introns of cerebellar-specific transcripts arising mostly during human fetal brain development from the usage of alternative promoters, but it is maintained in the adult cerebellum. Overexpression of the transfected (ATTTC)58 insertion, but not (ATTTT)n, leads to abnormal nuclear RNA accumulation. Zebrafish embryos injected with RNA of the (AUUUC)58 insertion, but not (AUUUU)n, showed lethal developmental malformations. Together, these results establish an unstable repeat insertion in DAB1 as a cause of cerebellar degeneration; on the basis of the genetic and phenotypic evidence, we propose this mutation as the molecular basis for SCA37.We thank the families who participated in this study. We are grateful to Goncalo Abecasis, Miguel Costa, Tito Vieira, and Andre Torres for help with MERLIN analysis; Beatriz Sobrino, Jorge Amigo, and Pilar Cacheiro for next-generation sequencing analysis, performed at the Santiago de Compostela node of the Spanish National Genotyping Center; Nuno Santarem and Anabela Cordeiro-da-Silva for assistance with cloning; Antonio Amorim, Laura Vilarinho, and Paula Jorge for samples from the Portuguese population; and Paula Magalhaes from the Institute for Molecular and Cell Biology Cell Culture and Genotyping Core for DNA extraction. This work was financed by Fundo Europeu de Desenvolvimento Regional (FEDER) funds through the COMPETE 2020 Operational Program for Competitiveness and Internationalization (POCI) of Portugal 2020 and by Portuguese funds through the Fundacao para a Ciencia e a Tecnologia (FCT) and Ministerio da Ciencia, Tecnologia, e Inovacao in the framework of the project "Institute for Research and Innovation in Health Sciences" (POCI-01-0145-FEDER-007274); and by FCT grant PTDC/SAU-GMG/098305/2008 to I.S. A. I.S. was the recipient of an FCT scholarship (SFRH/BD/30702/2006). J.R.L. was supported by scholarships from PEst-C/SAU/LA0002/2013 and the European Molecular Biology Organization (ASTF494-2015). C.L.O. was supported by a scholarship from PEst-C/SAU/LA0002/2013. This work was also financed by the Porto Neurosciences and Neurologic Disease Research Initiative at the Instituto de Investigacao e Inovacao em Saude (Norte-01-0145-FEDER-000008), supported by Norte Portugal Regional Operational Programme (NORTE 2020) under the PORTUGAL 2020 Partnership Agreement through FEDER, and by the Fondo de Investigacion Sanitaria of the Instituto de Salud Carlos III (grant PI12/00742)