991 resultados para Education . Progressions. Functions
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Aquest projecte t la intenci d'identificar i analitzar els efectes de la introducci d'Internet a les escoles catalanes (educaci primria i secundria). L'objectiu s posar de manifest la manera com s'utilitza la xarxa en aquest mbit i en quina mesura contribueix a l'aparici, en els centres educatius, d'una nova cultura adaptada a les necessitats de la societat xarxa. Amb aquest propsit, aquest projecte desplega les seves lnies d'anlisi per a fer atenci al procs d'incorporaci d'Internet, principalment, en tres direccions: la prctica pedaggica, les formes d'organitzaci i gesti dels centres educatius i la seva vinculaci amb la comunitat i el territori. Aquesta investigaci ha estat desenvolupada pel grup de recerca ENS (Education and Network Society). Amb una perspectiva comparativa, el treball d'aquest grup vol contribuir, sobre la base de dades empriques, a interpretar la transformaci de l'mbit educatiu no universitari en els parmetres que estableix, avui dia, la nostra societat.
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Functional Data Analysis (FDA) deals with samples where a whole function is observedfor each individual. A particular case of FDA is when the observed functions are densityfunctions, that are also an example of infinite dimensional compositional data. In thiswork we compare several methods for dimensionality reduction for this particular typeof data: functional principal components analysis (PCA) with or without a previousdata transformation and multidimensional scaling (MDS) for diferent inter-densitiesdistances, one of them taking into account the compositional nature of density functions. The difeerent methods are applied to both artificial and real data (householdsincome distributions)
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PURPOSE: Low socioeconomic status is associated with higher prevalence of diabetes, worse outcomes, and worse quality of care. We explored the relationship between education, as a measure of socioeconomic status, and quality of care in the Swiss context. PATIENTS AND METHODS: Data were drawn from a population-based survey of 519 adults with diabetes during fall 2011 and summer 2012 in a canton of Switzerland. We assessed patients and diabetes characteristics. Eleven indicators of quality of care were considered (six of process and five of outcomes of care). After bivariate analyses, regression analyses adjusted for age, sex, and diabetic complications were performed to assess the relationship between education and quality of care. RESULTS: Of 11 quality-of-care indicators, three were significantly associated with education: funduscopy (patients with tertiary versus primary education were more likely to get the exam: odds ratio, 1.8; 95% confidence interval [CI], 1.004-3.3) and two indicators of health-related quality of life (patients with tertiary versus primary education reported better health-related quality of life: Audit of Diabetes-Dependent Quality of Life: β=0.6 [95% CI, 0.2-0.97]; SF-12 mean physical component summary score: β=3.6 [95% CI, 0.9-6.4]). CONCLUSION: Our results suggest the presence of educational inequalities in quality of diabetes care. These findings may help health professionals focus on individuals with increased needs to decrease health inequalities.
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Compositional data analysis motivated the introduction of a complete Euclidean structure in the simplex of D parts. This was based on the early work of J. Aitchison (1986) and completed recently when Aitchinson distance in the simplex was associated with an inner product and orthonormal bases were identified (Aitchison and others, 2002; Egozcue and others, 2003). A partition of the support of a random variable generates a composition by assigning the probability of each interval to a part of the composition. One can imagine that the partition can be refined and the probability density would represent a kind of continuous composition of probabilities in a simplex of infinitely many parts. This intuitive idea would lead to a Hilbert-space of probability densitiesby generalizing the Aitchison geometry for compositions in the simplex into the set probability densities
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Rsum : c-Myc, le premier facteur de transcription de la famille Myc a t dcouvert il y a maintenant trente ans. Il reste l'heure actuelle parmi les plus puissants proto-oncognes connus. c-Myc est drgul dans plus de 50% des cancers, o il promeut la prolifration, la croissance cellulaire, et la noangiogense. Myc peut aussi influencer de nombreuses autres fonctions de par sa capacit activer ou rprimer la transcription de nombreux gnes, et agir globalement sur le gnome travers des modifications pigntiques de la chromatine. La famille d'oncognes Myc comprend, chez les mammifres, trois protines structurellement proches: c-Myc, N-Myc et L-Myc. Ces protines ont les mmes propriets biochimiques, exercent les mmes fonctions mais sont le plus souvent exprimes de faon mutuellement exclusive. Myc a t rcemment identifi comme un facteur clef dans la maintenance des cellules souches embryonnaires et adultes ainsi que dans la racquisition des propriets des cellules souches. Nous avons prcdemment dmontr que l'limination de c-Myc provoque une accumulation de cellules souches hmatopotiques (CSH) suite un dfaut de diffrenciation li la niche. Les CSH sont responsables de la production de tous les lments cellulaires du sang pour toute la vie de l'individu et sont dfinies par leur capacit s'auto-renouveler tout en produisant des prcurseurs hmatopotiques. Afin de mieux comprendre la fonction de Myc dans les CSH, nous avons choisi de combiner l'utilisation de modles de souris gntiquement modifies une caractrisation systmatique des schmas d'expression de c-Myc, N-Myc et L-Myc dans tout le systme hmatopotique. Nous avons ainsi dcouvert que les CSH les plus immatures expriment des quantits quivalentes de transcrits de c-myc et N-myc. Si les CSH dficientes en N-myc seulement ont une capacit d'auto-renouvellement long-terme rduite, l'invalidation combine des gnes c-myc et N-myc conduit une pan-cytopnie suivie d'une mort rapide de l'animal, pour cause d'apoptose de tous les types cellulaires hmatopotiques. En particulier, les CSH en cours d'auto-renouvelemment, mais pas les CSH quiescentes, accumulent du Granzyme B (GrB), une molcule fortement cytotoxique qui provoque une mort cellulaire rapide. Ces donnes ont ainsi mis au jour un nouveau mcanisme dont dpend la survie des CSH, savoir la rpression du GrB, une enzyme typiquement utilise par le systme immunitaire inn pour liminer les tumeurs et les cellules infectes par des virus. Dans le but d'valuer l'tendue de la redondance entre c-Myc et N-Myc dans les CSH, nous avons d'une part examin des souris dans lesquelles les squences codantes de c-myc sont remplaces par celles de N-myc (NCR) et d'autre part nous avons gner une srie alllique de myc en liminant de faon combinatoire un ou plusieurs allles de c-myc et/ou de N-myc. Alors que l'analyse des souris NCR suggre que c-Myc et N-Myc sont qualitativement redondants, la srie alllique indique que les efficiences avec lesquelles ces deux protines influencent des procds essentiels la maintenance des CSH sont diffrentes. En conclusion, nos donnes gntiques montrent que l'activit gnrale de MYC, fournie par c-Myc et N-Myc, contrle plusieurs aspects cruciaux de la fonction des CSH, notamment l'auto-renouvellement, la survie et la diffrenciation. Abstract : c-Myc, the first Myc transcription factor was discovered 30 years ago and is to date one of the most potent proto-oncogenes described. It is found to be misregulated in over 50% of all cancers, where it drives proliferation, cell growth and neo-angiogenesis. Myc can also influence a variety of other functions, owing to its ability to activate and repress transcription of many target genes and to globally regulate the genome via epigenetic modifications of the chromatin. The Myc family of oncogenes consists of three closely related proteins in mammals: c-Myc, N-Myc and L-Myc. These proteins share the same biochemical properties, exert mostly the same functions, but are most often expressed in mutually exclusive patterns. Myc is now emerging as a key factor in maintenance of embryonic and adult stem cells as well as in reacquisition of stem cell properties, including induced reprogramming. We previously showed that c-Myc deficiency can cause the accumulation of hematopoietic stem cells (HSCs) due to a niche dependent differentiation defect. HSCs are responsible for life-long replenishment of all blood cell types, and are defined by their ability to self-renew while concomitantly giving rise to more commited progenitors. To gain further insight into the function of Myc in HSCs, in this study we combine the use of genetically-modified mouse models with the systematic characterization of c-myc, N-myc and L-myc transcription patterns throughout the hematopoietic system. Interestingly, the most immature HSCs express not only c-myc, but also about equal amounts of N-myc transcripts. Although conditional deletion of N-myc alone in the bone marrow does not affect steady-state hematopoiesis, N-myc null HSCs show impaired long-term self-renewal capacity. Strikingly, combined deficiency of c-Myc and N-Myc results in pan-cytopenia and rapid lethality, due to the apoptosis of most hematopoietic cell types. In particular, self-renewing HSCs, but not quiescent HSCs or progenitor cell types rapidly up-regulate and accumulate the potent cytotoxic molecule GranzymeB (GrB), causing their rapid cell death. These data uncover a novel pathway on which HSC survival depends on, namely repression of GrB, a molecule typically used by the innate immune system to eliminate tumor and virus infected cells. To evaluate the extent of redundancy between c-Myc and N-Myc in HSCs, we examined mice in which c-myc coding sequences are replaced by that of N-myc (NCR) and also generated an allelic series of myc, by combinatorially deleting one or several c-myc and/or N-myc alleles. While the analysis of NCR mice suggests that c-Myc and N-Myc are qualitatively functionally redundant, our allelic series indicates that the efficiencies with which these two proteins affect crucial HSC maintenance processes are likely to be distinct. Collectively, our genetic data show that general "MYC" activity delivered by c-Myc and N-Myc controls crucial aspects of HSC function, including self-renewal, survival and niche dependent differentiation.
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The polymeric Ig receptor (pIgR) ensures efficient secretion of polymeric IgA (pIgA) at mucosal surfaces. On basal to apical transport across epithelial cells, the pIgR extracellular domain is cleaved, releasing secretory component (SC) in association with pIgA. This finds its raison d'tre in the recent observation that SC is directly involved in the protective function of secretory IgA. In addition, free SC exhibits scavenger properties with respect to enteric pathogens. However, although pIgR dedicates its life to mucosal protection, it also seems to permit pathogen entrance through the epithelial barrier. The multiple mechanisms that they are involved in make pIgR and SC instrumental to mucosal immunity.
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Teaching and research are organised differently between subject domains: attempts to construct typologies of higher education institutions, however, often do not include quantitative indicators concerning subject mix which would allow systematic comparisons of large numbers of higher education institutions among different countries, as the availability of data for such indicators is limited. In this paper, we present an exploratory approach for the construction of such indicators. The database constructed in the AQUAMETH project, which includes also data disaggregated at the disciplinary level, is explored with the aim of understanding patterns of subject mix. For six European countries, an exploratory and descriptive analysis of staff composition divided in four large domains (medical sciences, engineering and technology, natural sciences and social sciences and humanities) is performed, which leads to a classification distinguishing between specialist and generalist institutions. Among the latter, a further distinction is made based on the presence or absence of a medical department. Preliminary exploration of this classification and its comparison with other indicators show the influence of long term dynamics on the subject mix of individual higher education institutions, but also underline disciplinary differences, for example regarding student to staff ratios, as well as national patterns, for example regarding the number of PhD degrees per 100 undergraduate students. Despite its many limitations, this exploratory approach allows defining a classification of higher education institutions that accounts for a large share of differences between the analysed higher education institutions.
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J. Neurochem. (2010) 10.1111/j.1471-4159.2010.06935.x Abstract Apart of its well known function of 'energetic buffer' through the creatine/phosphocreatine/creatine kinase system allowing the regeneration of ATP, creatine has been recently suggested as a potential neuromodulator of even true neurotransmitter. Moreover, the recent discovery of primary creatine deficiency syndromes, due to deficiencies in l-arginine : glycine amidinotransferase or guanidinoacetate methyltransferase (the two enzymes allowing creatine synthesis) or in the creatine transporter, has shed new light on creatine synthesis, metabolism and transport, in particular in CNS which appears as the main tissue affected by these creatine deficiencies. Recent data suggest that creatine can cross blood-brain barrier but only with a poor efficiency, and that the brain must ensure parts of its needs in creatine by its own endogenous synthesis. Finally, the recent years have demonstrated the interest to use creatine as a neuroprotective agent in a growing number of neurodegenerative diseases, including Parkinson's and Huntington's diseases. This article aims at reviewing the latest data on creatine metabolism and transport in the brain, in relation to creatine deficiencies and to the potential use of creatine as neuroprotective molecule. Emphasis is also given to the importance of creatine for cerebral function.
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Peroxisome proliferator-activated receptors (PPARs) compose a family of three nuclear receptors which act as lipid sensors to modulate gene expression. As such, PPARs are implicated in major metabolic and inflammatory regulations with far-reaching medical consequences, as well as in important processes controlling cellular fate. Throughout this review, we focus on the cellular functions of these receptors. The molecular mechanisms through which PPARs regulate transcription are thoroughly addressed with particular emphasis on the latest results on corepressor and coactivator action. Their implication in cellular metabolism and in the control of the balance between cell proliferation, differentiation and survival is then reviewed. Finally, we discuss how the integration of various intra-cellular signaling pathways allows PPARs to participate to whole-body homeostasis by mediating regulatory crosstalks between organs.
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BACKGROUND The lysophosphatidic acid LPA receptor regulates plasticity and neurogenesis in the adult hippocampus. Here, we studied whether absence of the LPA receptor modulated the detrimental effects of chronic stress on hippocampal neurogenesis and spatial memory. METHODOLOGY/PRINCIPAL FINDINGS Male LPA-null (NULL) and wild-type (WT) mice were assigned to control or chronic stress conditions (21 days of restraint, 3 h/day). Immunohistochemistry for bromodeoxyuridine and endogenous markers was performed to examine hippocampal cell proliferation, survival, number and maturation of young neurons, hippocampal structure and apoptosis in the hippocampus. Corticosterone levels were measured in another a separate cohort of mice. Finally, the hole-board test assessed spatial reference and working memory. Under control conditions, NULL mice showed reduced cell proliferation, a defective population of young neurons, reduced hippocampal volume and moderate spatial memory deficits. However, the primary result is that chronic stress impaired hippocampal neurogenesis in NULLs more severely than in WT mice in terms of cell proliferation; apoptosis; the number and maturation of young neurons; and both the volume and neuronal density in the granular zone. Only stressed NULLs presented hypocortisolemia. Moreover, a dramatic deficit in spatial reference memory consolidation was observed in chronically stressed NULL mice, which was in contrast to the minor effect observed in stressed WT mice. CONCLUSIONS/SIGNIFICANCE These results reveal that the absence of the LPA receptor aggravates the chronic stress-induced impairment to hippocampal neurogenesis and its dependent functions. Thus, modulation of the LPA receptor pathway may be of interest with respect to the treatment of stress-induced hippocampal pathology.
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BACKGROUND Extreme weight conditions (EWC) groups along a continuum may share some biological risk factors and intermediate neurocognitive phenotypes. A core cognitive trait in EWC appears to be executive dysfunction, with a focus on decision making, response inhibition and cognitive flexibility. Differences between individuals in these areas are likely to contribute to the differences in vulnerability to EWC. The aim of the study was to investigate whether there is a common pattern of executive dysfunction in EWC while comparing anorexia nervosa patients (AN), obese subjects (OB) and healthy eating/weight controls (HC). METHODS Thirty five AN patients, fifty two OB and one hundred thirty seven HC were compared using the Wisconsin Card Sorting Test (WCST); Stroop Color and Word Test (SCWT); and Iowa Gambling Task (IGT). All participants were female, aged between 18 and 60 years. RESULTS There was a significant difference in IGT score (F(1.79); p<.001), with AN and OB groups showing the poorest performance compared to HC. On the WCST, AN and OB made significantly more errors than controls (F(25.73); p<.001), and had significantly fewer correct responses (F(2.71); p<.001). Post hoc analysis revealed that the two clinical groups were not significantly different from each other. Finally, OB showed a significant reduced performance in the inhibition response measured with the Stroop test (F(5.11); p<.001) compared with both AN and HC. CONCLUSIONS These findings suggest that EWC subjects (namely AN and OB) have similar dysfunctional executive profile that may play a role in the development and maintenance of such disorders.
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A cause and effect relationship between arterial hypertension and decline of cognitive function has long been suspected. In middle-age subjects indeed, an abnormally high blood pressure is a risk factor for the long-term development of dementia. Presently, it seems crucial to treat hypertensive patients in order to better protect them against cognitive decline. However, in the elderly patients the risk of mental deterioration may also be enhanced when diastolic pressure becomes too low, for example below 70 mmHg. Further studies are required to better define the antihypertensive drug regimen and target blood pressure which would be optimal for the prevention of cerebral small vessel disease.