1000 resultados para Diner -- Aspectes psicològics
Resumo:
La classificació inicial dels penats és transcendental pel fet que representa la primera proposta o disseny de tractament de l’intern, i constitueix la primera valoració del risc del subjecte. La intenció de la recerca ha estat, doncs, establir un model orientatiu d’entrevista de classificació inicial, la valoració dels aspectes significatius del risc i, de resultes, produir una guia o model d’informe, per tal d’homogeneïtzar i dotar el col·lectiu de pautes comunes d’actuació. Aquest objectiu s’ha tractat d’assolir cercant l’equilibri entre la qualitat i la simplicitat i essent conscients que el document final ha de ser una eina operativa i facilitadora de la tasca professional. El document produït pretén establir pautes d’actuació de mínims que garanteixin una uniformitat en la valoració i una aportació bàsica de dades rellevants a les autoritats administratives o judicials que han de resoldre en diferents instàncies aspectes relatius a la classificació inicial dels penats. El document s’acompanya de material d’avaluació que, tot i no estar dissenyat específicament per a poblacions penitenciàries, per les seves característiques de brevetat i simplicitat de passació i d’interpretació, pot resultar molt pràctic per aprofundir en algunes qüestions especifiques de l’avaluació quan sigui necessari.
Resumo:
El projecte que s’ha presentat correspon a la titulació d’Enginyeria en Informàtica i conté diversos aspectes relacionats al desenvolupament d’una aplicació web per a gestionar els pressupostos de l’empresa Ncora. Es presenta un estudi i anàlisi de requeriments, una compra de servidors, una instal·lació i configuració dels servidors en l’entorn hardware del núvol de Ncora, un anàlisi i disseny de la base de dades i un desenvolupament a mida de l’aplicació software. L’objectiu principal del projecte és l’estalvi de temps en la creació de pressupostos i la ràpida cerca de pressupostos fets així com dels seus components.
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Fertility has unanimously declined across the entire post-communist region. This study explores the variation in fertility trends over time among these countries and assesses to what degree three explanations are applicable: second demographic transition (SDT), postponement transition (PPT) or reaction to the economic crisis. Moreover, on the basis of SDT and PPT theoretical tenets, as well as descriptive evidence, the economic context is hypothesized to be linked to two processes of fertility decline conversely. The results show that no one theoretical explanation is sufficient to explain the complex fertility declines across the entire post-communist region from 1990 to 2003. In some countries, a great part of the decline in fertility occurred before significant postponement of childbearing began, which indicates that the dramatic decline was due to stopping behavior or postponement of higher order births. Postponement of first births, either through PPT or SDT processes, greatly contributed to fertility decline in a small number of countries. Pooled cross-sectional time-series analyses of age-specific birthrates confirm that these two distinct processes are present and show that the economic crisis explanation has explanatory power for declining birth rates. In contrast, logistic regressions show that the likelihood of postponing childbirth increases with improved economic conditions. These results confirm the importance of taking the economic context into account when discussing explanations for fertility decline. More specifically, the results indicate that the severity and duration of economic crisis, or absence thereof, influenced the extent and manner in which fertility declined.
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This study engages with the debate over the mortality crises in the former Soviet Union and Central and Eastern Europe by 1) considering at length and as complementary to each other the two most prominent explanations for the post-communist mortality crisis, stress and alcohol consumption; 2) emphasizing the importance of context by exploiting systematic similarities and differences across the region. Differential mortality trajectories reveal three country groups that cluster both spatially and in terms of economic transition experiences. The first group are the countries furthest west in which mortality rates increased minimally after the transition began. The second group experienced a severe increase in mortality rates in the early 1990s, but recovered previous levels within a few years. These countries are located peripherally to Russia and its nearest neighbours. The final group consists of countries that experienced two mortality increases or in which mortality levels had not recovered to pre-transition levels well into the 21st century. Cross-sectional time-series data analyses of men’s and women’s age and cause-specific death rates reveal that the clustering of these countries and their mortality trajectories can be partially explained by the economic context, which is argued to be linked to stress and alcohol consumption. Above and beyond many basic differences in the country groups that are held constant—including geographically and historically shared cultural, lifestyle and social characteristics—poor economic conditions account for a remarkably consistent share of excess age-specific and cause-specific deaths.
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Background: This paper analyses gender inequalities in health status and in social determinants of health among the elderly in Western Europe. Methods: Data came from the first wave of the “Survey of Health, Ageing and Retirement in Europe” (SHARE, 2004). For the purposes of this study a subsample of community-residing people aged 65-85 years with no paid work was selected (4218 men and 5007 women). Multiple logistic regression models separated by sex and adjusted for age and country were fitted. Results: Women were more likely to report poor health status, limitations in mobility and poor mental health. Whereas in both sexes educational attainment was associated with the three health indicators, household income was only related to poor self-rated health among women. The relationship between living arrangements and health differed by gender and was primarily associated with poor mental health. In both sexes, not living with the partner but living with other people and being the household head was related to poor mental health status (aOR=2.14; 95% CI=1.11-4.14 for men and aOR=1.75; 95% CI=1.12-2.72 for women). Additionally, women living with their partner and other(s) and those living alone were more likely to report poor mental health status (aOR=1.67; 95% CI=1.17-2.41 and aOR=1.58; 95% CI=1.26-1.97, respectively). Conclusions: Health inequalities persist among the elderly. Women have poorer health status than men and in both sexes the risk of poor health status increases among those with low educational attainment. Living arrangements are primarily associated with poor mental health status with patterns that differ by gender.
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This study analyses gender inequalities in health among elderly people in Catalonia (Spain) by adopting a conceptual framework that globally considers three dimensions of health determinants : socio-economic position, family characteristics and social support. Data came from the 2006 Catalonian Health Survey. For the purposes of this study a sub-sample of people aged 65–85 years with no paid job was selected (1,113 men and 1,484 women). The health outcomes analysed were self-perceived health status, poor mental health status and long-standing limiting illness. Multiple logistic regression models separated by sex were fitted and a hierarchical model was fitted in three steps. Health status among elderly women was poorer than among the men for the three outcomes analysed. Whereas living with disabled people was positively related to the three health outcomes and confidant social support was negatively associated with all of them in both sexes, there were gender differences in other social determinants of health. Our results emphasise the importance of using an integrated approach for the analysis of health inequalities among elderly people, simultaneously considering socio-economic position, family characteristics and social support, as well as different health indicators, in order fully to understand the social determinants of the health status of older men and women.
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This study assesses the decline in second birth rates for men and women across different skill levels in transitional Russia. Changes within educational groups and occupational classes are observed over three distinct time periods: the Soviet era, economic crisis, and economic recovery. The most remarkable finding is the similarity in the extent second birth rates declined within educational groups and occupational classes during the economic crisis. Although further decline occurred in the recovery period, more variation emerged across groups.
Resumo:
En este artículo se aportan algunos de los resultados preliminares de mi tesis doctoral: “Las políticas públicas de la televisión digital terrestre en la Unión Europea. Estudio comparado de Suecia y España”. Mediante el análisis de las estructuras institucionales implicadas en la transición analógico-digital de la plataforma de difusión terrestre, sus lógicas legitimadoras y las estrategias desarrolladas, se pretende contribuir a la identificación de buenas prácticas y de factores clave de éxito que ayuden a diseñar políticas públicas más efectivas.
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La idea de que el lenguaje ha transformado la conciencia humana porque permite el desarrollo de nuevas formas de pensamiento y la adquisición de conocimientos, nos lleva a buscar una explicación teórica sobre las relaciones existentes entre el pensamiento, lenguaje y su posible relación en la determinación de acciones de un receptor. En este escrito sepresenta un análisis teórico sobre algunos conceptos que componen el lenguaje y su potencial injerencia en los procesos de comunicación social.
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BACKGROUND: Selenoproteins are a diverse family of proteins notable for the presence of the 21st amino acid, selenocysteine. Until very recently, all metazoan genomes investigated encoded selenoproteins, and these proteins had therefore been believed to be essential for animal life. Challenging this assumption, recent comparative analyses of insect genomes have revealed that some insect genomes appear to have lost selenoprotein genes. METHODOLOGY/PRINCIPAL FINDINGS: In this paper we investigate in detail the fate of selenoproteins, and that of selenoprotein factors, in all available arthropod genomes. We use a variety of in silico comparative genomics approaches to look for known selenoprotein genes and factors involved in selenoprotein biosynthesis. We have found that five insect species have completely lost the ability to encode selenoproteins and that selenoprotein loss in these species, although so far confined to the Endopterygota infraclass, cannot be attributed to a single evolutionary event, but rather to multiple, independent events. Loss of selenoproteins and selenoprotein factors is usually coupled to the deletion of the entire no-longer functional genomic region, rather than to sequence degradation and consequent pseudogenisation. Such dynamics of gene extinction are consistent with the high rate of genome rearrangements observed in Drosophila. We have also found that, while many selenoprotein factors are concomitantly lost with the selenoproteins, others are present and conserved in all investigated genomes, irrespective of whether they code for selenoproteins or not, suggesting that they are involved in additional, non-selenoprotein related functions. CONCLUSIONS/SIGNIFICANCE: Selenoproteins have been independently lost in several insect species, possibly as a consequence of the relaxation in insects of the selective constraints acting across metazoans to maintain selenoproteins. The dispensability of selenoproteins in insects may be related to the fundamental differences in antioxidant defense between these animals and other metazoans.
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Background: GTF2I codes for a general intrinsic transcription factor and calcium channel regulator TFII-I, with high and ubiquitous expression, and a strong candidate for involvement in the morphological and neuro-developmental anomalies of the Williams-Beuren syndrome (WBS). WBS is a genetic disorder due to a recurring deletion of about 1,55-1,83 Mb containing 25-28 genes in chromosome band 7q11.23 including GTF2I. Completed homozygous loss of either the Gtf2i or Gtf2ird1 function in mice provided additional evidence for the involvement of both genes in the craniofacial and cognitive phenotype. Unfortunately nothing is now about the behavioral characterization of heterozygous mice. Methods: By gene targeting we have generated a mutant mice with a deletion of the first 140 amino-acids of TFII-I. mRNA and protein expression analysis were used to document the effect of the study deletion. We performed behavioral characterization of heterozygous mutant mice to document in vivo implications of TFII-I in the cognitive profile of WBS patients. Results: Homozygous and heterozygous mutant mice exhibit craniofacial alterations, most clearly represented in homozygous condition. Behavioral test demonstrate that heterozygous mutant mice exhibit some neurobehavioral alterations and hyperacusis or odynacusis that could be associated with specific features of WBS phenotype. Homozygous mutant mice present highly compromised embryonic viability and fertility. Regarding cellular model, we documented a retarded growth in heterozygous MEFs respect to homozygous or wild-type MEFs. Conclusion: Our data confirm that, although additive effects of haploinsufficiency at several genes may contribute to the full craniofacial or neurocognitive features of WBS, correct expression of GTF2I is one of the main players. In addition, these findings show that the deletion of the fist 140 amino-acids of TFII-I altered it correct function leading to a clear phenotype, at both levels, at the cellular model and at the in vivo model.
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Background: Two genes are called synthetic lethal (SL) if mutation of either alone is not lethal, but mutation of both leads to death or a significant decrease in organism's fitness. The detection of SL gene pairs constitutes a promising alternative for anti-cancer therapy. As cancer cells exhibit a large number of mutations, the identification of these mutated genes' SL partners may provide specific anti-cancer drug candidates, with minor perturbations to the healthy cells. Since existent SL data is mainly restricted to yeast screenings, the road towards human SL candidates is limited to inference methods. Results: In the present work, we use phylogenetic analysis and database manipulation (BioGRID for interactions, Ensembl and NCBI for homology, Gene Ontology for GO attributes) in order to reconstruct the phylogenetically-inferred SL gene network for human. In addition, available data on cancer mutated genes (COSMIC and Cancer Gene Census databases) as well as on existent approved drugs (DrugBank database) supports our selection of cancer-therapy candidates.Conclusions: Our work provides a complementary alternative to the current methods for drug discovering and gene target identification in anti-cancer research. Novel SL screening analysis and the use of highly curated databases would contribute to improve the results of this methodology.
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Background: Lynch syndrome (LS) is an autosomal dominant inherited cancer syndrome characterized by early onset cancers of the colorectum, endometrium and other tumours. A significant proportion of DNA variants in LS patients are unclassified. Reports on the pathogenicity of the c.1852_1853AA>GC (p.Lys618Ala) variant of the MLH1 gene are conflicting. In this study, we provide new evidence indicating that this variant has no significant implications for LS.Methods: The following approach was used to assess the clinical significance of the p.Lys618Ala variant: frequency in a control population, case-control comparison, co-occurrence of the p.Lys618Ala variant with a pathogenic mutation, co-segregation with the disease and microsatellite instability in tumours from carriers of the variant. We genotyped p.Lys618Ala in 1034 individuals (373 sporadic colorectal cancer [CRC] patients, 250 index subjects from families suspected of having LS [revised Bethesda guidelines] and 411 controls). Three well-characterized LS families that fulfilled the Amsterdam II Criteria and consisted of members with the p.Lys618Ala variant were included to assess co-occurrence and co-segregation. A subset of colorectal tumour DNA samples from 17 patients carrying the p.Lys618Ala variant was screened for microsatellite instability using five mononucleotide markers.Results: Twenty-seven individuals were heterozygous for the p.Lys618Ala variant; nine had sporadic CRC (2.41%), seven were suspected of having hereditary CRC (2.8%) and 11 were controls (2.68%). There were no significant associations in the case-control and case-case studies. The p.Lys618Ala variant was co-existent with pathogenic mutations in two unrelated LS families. In one family, the allele distribution of the pathogenic and unclassified variant was in trans, in the other family the pathogenic variant was detected in the MSH6 gene and only the deleterious variant co-segregated with the disease in both families. Only two positive cases of microsatellite instability (2/17, 11.8%) were detected in tumours from p.Lys618Ala carriers, indicating that this variant does not play a role in functional inactivation of MLH1 in CRC patients.Conclusions: The p.Lys618Ala variant should be considered a neutral variant for LS. These findings have implications for the clinical management of CRC probands and their relatives.
Hypothalamus transcriptome profile suggests an anorexia-cachexia syndrome in the anx/anx mouse model
Resumo:
The anx/anx mouse displays poor appetite and lean appearance and is considered a good model for the study of anorexia nervosa. To identify new genes involved in feeding behavior and body weight regulation we performed an expression profiling in the hypothalamus of the anx/anx mice. Using commercial microarrays we detected 156 differentially expressed genes and validated 92 of those using TaqMan low-density arrays. The expression of a set of 87 candidate genes selected based on literature evidences was also quantified by TaqMan low-density arrays. Our results showed enrichment in deregulated genes involved in cell death, cell morphology and cancer as well as an alteration of several signaling circuits involved in energy balance including neuropeptide Y and melanocortin signaling. The expression profile along with the phenotype led us to conclude that anx/anx mice resemble the anorexia-cachexia syndrome typically observed in cancer, infection with human immunodeficiency virus or chronic diseases, rather than starvation, and that anx/anx mice could be considered a good model for the treatment and investigation of this condition.
Resumo:
Eating disorders (EDs) are complex psychiatric diseases that include anorexia nervosa and bulimia nervosa, and have higher than 50% heritability. Previous studies have found association of BDNF and NTRK2 to ED, while animal models suggest that other neurotrophin genes might also be involved in eating behavior. We have performed a family-based association study with 151 TagSNPs covering 10 neurotrophin signaling genes: NGFB, BDNF, NTRK1, NGFR/p75, NTF4/5, NTRK2, NTF3, NTRK3, CNTF and CNTFR in 371 ED trios of Spanish, French and German origin. Besides several nominal associations, we found a strong significant association after correcting for multiple testing (P = 1.04 × 10−4) between ED and rs7180942, located in the NTRK3 gene, which followed an overdominant model of inheritance. Interestingly, HapMap unrelated individuals carrying the rs7180942 risk genotypes for ED showed higher levels of expression of NTRK3 in lymphoblastoid cell lines. Furthermore, higher expression of the orthologous murine Ntrk3 gene was also detected in the hypothalamus of the anx/anx mouse model of anorexia. Finally, variants in NGFB gene appear to modify the risk conferred by the NTRK3 rs7180942 risk genotypes (P = 4.0 × 10−5) showing a synergistic epistatic interaction. The reported data, in addition to the previous reported findings for BDNF and NTRK2, point neurotrophin signaling genes as key regulators of eating behavior and their altered cross-regulation as susceptibility factors for EDs.