838 resultados para Non-genetic factors


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The Federal Institution for Education, Science and Technology, in its historical path, has been living different changes. The transformations occurred along the way have been determined by coercive forces from the institutional environment, which has became more and more broad and complex throughout the time, obtaining diverse characteristics and new elements such as non institutional factors1 which started to contribute with the other changes. In this context, this work aims to study the isomorphic practices of the managers in the institutional changes process of the IFRN in 1998 and 2008, as of a theoretical coevolutionary perspective (CHILD; RODRIGUES; LEWIN; CARROL; VOLBERDA, 2003). This theory brings a new point of view for the organization analysis to the organizational studies, since it offers a non deterministic and non linear lection of the evolution process, which means, a coevolution. Thus, the organizations and their institutional and non institutional environment auto evolve, auto organize and auto reproduce. Therefore, the institutional and non institutional factors of the macro environment keep a continuous interdependence relationship with the organizations. For the means of this study, it is important to understand that is impossible to comprehend the object, the isomorphic practices, without considering that the previous institutional changes and its evolutions, its continuations and discontinuations, important in the coevolution process. As such, to call upon the institutional historical track is a fundamental aspect to materialize this study, for the recursive movement is indeed present in the coevolution. Another important point to make this research effective is that it is not possible to abdicate from the hologramatic view2 of this study, which considers the object, the isomorphic practices, part of the whole and this whole is also in the parts, therefore it is impossible to comprehend the object of study outside the context where it belongs. With this, as of the objective previously proposed, it is necessary to describe the characteristics of coevolution of the institutional changes related in 1998 and 2008; analyze the dynamic of the isomorphic mechanisms in its respective institutional change process; and describe the lessons learned which the isomorphic practices left to the IFRN, regarding its benefits and difficulties. All these transformations happened through coercive forces3 of the institutional environment. As of the Nineties, these forces became stronger, the environment became broader and more complex, with the emergency of new environmental factors. This study proposed to study the managing process and its practices, related to the micro environment, although it is required to articulate these actions, the demands and requirements from the macro environment. To make this research effective, semi structured interviews have been conducted with the managers who participated in both institutional change processes. In the results analysis, it has been possible to verify the particularity of each change, the one from 1998 with a strong normative action of the managers against coercive forces from the government for the search of recognition and the institutional legitimation and the one in 2008, which has been characterized by the normative action by managers in agreement with the coercive forces from the government, in favor of the government policy for the technological professional education. However, the results analysis it is possible to notice the evidence of a belonging feeling from the interviewed managers

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Familial amyloid polyneuropathy (FAP) or paramiloidosis is an autosomal dominant neurodegenerative disease with onset on adult age that is characterized by mutated protein deposition in the form of amyloid substance. FAP is due to a point alteration in the transthyretin (TTR) gene and until now more than 100 amyloidogenic mutations have been described in TTR gene. FAP shows a wide variation in age-at-onset (AO) (19-82 years, in Portuguese cases) and the V30M mutation often runs through several generation of asymptomatic carriers, before expressing in a proband, but the protective effect disappear in a single generation, with offspring of late-onset cases having early onset. V30M mutation does not explain alone the symptoms and AO variability of the disease observed in the same family. Our aim in this study was to identify genetic factors associated with AO variability and reduced penetrance which can have important clinical implications. To accomplish this we genotyped 230 individuals, using a directautomated sequencing approach in order to identify possible genetic modifiers within the TTR locus. After genotyping, we assessed a putative association of the SNPs found with AO and an intensive in silico analysis was performed in order to understand a possible regulation of gene expression. Although we did not find any significant association between SNPs and AO, we found very interesting and unreported results in the in silico analysis since we observed some alterations in the mechanism of splicing, transcription factors binding and miRNAs binding. All of these mechanisms when altered can lead to dysregulation of gene expression, which can have an impact in AO and phenotypic variability. These putative mechanisms of regulation of gene expression within the TTR gene could be used in the future as potential therapeutical targets, and could improve genetic counselling and follow-up of mutation carriers.

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Das starke wissenschaftliche Interesse an der relativen Bedeutung genetischer Faktoren und variabler Umweltbedingungen für die Genese interindividueller Persönlichkeitsunterschiede hat in den letzten Jahren zu einer Intensivierung der Zwillings- und Adoptionsforschung geführt. In den meisten dieser Arbeiten wurden und werden bevorzugt Intelligenztests und Persönlichkeitsfragebogen verwendet. Dabei handelt es sich durchweg um Querschnittstudien. Im Vergleich dazu erstreckt sich die Gottschaldsche Längsschnittstudie an eineiigen und zweieiigen Zwillingen inzwischen auf einen Zeitraum von über 55 Jahren. Hinzu kommt, daß neben quantitativen Informationen auch vielfältige qualitative Daten aus Beobachtungen und Befragungen der Probanden verfügbar sind. (DIPF/Orig.)

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This PhD thesis contains three main chapters on macro finance, with a focus on the term structure of interest rates and the applications of state-of-the-art Bayesian econometrics. Except for Chapter 1 and Chapter 5, which set out the general introduction and conclusion, each of the chapters can be considered as a standalone piece of work. In Chapter 2, we model and predict the term structure of US interest rates in a data rich environment. We allow the model dimension and parameters to change over time, accounting for model uncertainty and sudden structural changes. The proposed timevarying parameter Nelson-Siegel Dynamic Model Averaging (DMA) predicts yields better than standard benchmarks. DMA performs better since it incorporates more macro-finance information during recessions. The proposed method allows us to estimate plausible realtime term premia, whose countercyclicality weakened during the financial crisis. Chapter 3 investigates global term structure dynamics using a Bayesian hierarchical factor model augmented with macroeconomic fundamentals. More than half of the variation in the bond yields of seven advanced economies is due to global co-movement. Our results suggest that global inflation is the most important factor among global macro fundamentals. Non-fundamental factors are essential in driving global co-movements, and are closely related to sentiment and economic uncertainty. Lastly, we analyze asymmetric spillovers in global bond markets connected to diverging monetary policies. Chapter 4 proposes a no-arbitrage framework of term structure modeling with learning and model uncertainty. The representative agent considers parameter instability, as well as the uncertainty in learning speed and model restrictions. The empirical evidence shows that apart from observational variance, parameter instability is the dominant source of predictive variance when compared with uncertainty in learning speed or model restrictions. When accounting for ambiguity aversion, the out-of-sample predictability of excess returns implied by the learning model can be translated into significant and consistent economic gains over the Expectations Hypothesis benchmark.

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This PhD thesis contains three main chapters on macro finance, with a focus on the term structure of interest rates and the applications of state-of-the-art Bayesian econometrics. Except for Chapter 1 and Chapter 5, which set out the general introduction and conclusion, each of the chapters can be considered as a standalone piece of work. In Chapter 2, we model and predict the term structure of US interest rates in a data rich environment. We allow the model dimension and parameters to change over time, accounting for model uncertainty and sudden structural changes. The proposed time-varying parameter Nelson-Siegel Dynamic Model Averaging (DMA) predicts yields better than standard benchmarks. DMA performs better since it incorporates more macro-finance information during recessions. The proposed method allows us to estimate plausible real-time term premia, whose countercyclicality weakened during the financial crisis. Chapter 3 investigates global term structure dynamics using a Bayesian hierarchical factor model augmented with macroeconomic fundamentals. More than half of the variation in the bond yields of seven advanced economies is due to global co-movement. Our results suggest that global inflation is the most important factor among global macro fundamentals. Non-fundamental factors are essential in driving global co-movements, and are closely related to sentiment and economic uncertainty. Lastly, we analyze asymmetric spillovers in global bond markets connected to diverging monetary policies. Chapter 4 proposes a no-arbitrage framework of term structure modeling with learning and model uncertainty. The representative agent considers parameter instability, as well as the uncertainty in learning speed and model restrictions. The empirical evidence shows that apart from observational variance, parameter instability is the dominant source of predictive variance when compared with uncertainty in learning speed or model restrictions. When accounting for ambiguity aversion, the out-of-sample predictability of excess returns implied by the learning model can be translated into significant and consistent economic gains over the Expectations Hypothesis benchmark.

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Dissertação de Mestrado, Tecnologia e Segurança Alimentar, 4 de Abril de 2016, Universidade dos Açores.

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Although stable isotope ratios are increasingly used to investigate the trophic ecology of marine organisms, their spatial variations are still poorly understood in the coastal environment. In this study, we measured the stable isotope composition (δ13C, δ15N) of suspended particulate organic matter (SPOM) (primary producer), a suspension feeder, the great scallop Pecten maximus (primary consumer), megabenthic decapods and benthic fishes (secondary consumers) along a depth gradient (from 5m to 155m depth) across the continental shelf of the Bay of Biscay. Although the three trophic levels exhibited similar δ13C patterns along the gradient, the δ15N patterns varied between SPOM, scallops and carnivores. The δ15N difference between SPOM and scallops decreased with increasing depth, suggesting that non trophic factors may affect the stable isotope composition of scallops at deepest sampling stations. An opposed trend was found between scallops and carnivores, suggesting that the trophic level of these carnivores increased at higher depth, possibly as an adaptation to lower prey abundances. Although our results suggest that primary consumers are suitable to establish isotopic baselines in coastal environments, we stress the need for further studies aiming at characterizing the variability of stable isotopes in coastal biota, and the respective effects of baseline, trophic and metabolic factors in their isotopic composition.

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Autism Spectrum Disorder (ASD) is a frequent and complex neurodevelopmental disorder, characterized by impairments in social communication and repetitive behaviors and with a high male to female ratio: ~4:1. Genetic factors, including rare Copy Number Variants (CNVs), have a substantial impact in ASD risk1, and are associated with specific phenotypic manifestations2. Recent studies reported that rare inherited CNVs are enriched in mothers of ASD children compared with mothers of controls and are preferentially transmitted from mothers to ASD children suggesting a sex bias in CNV transmission; further, the imbalanced transmission of small pathogenic CNVs from unaffected mothers to their sons with ASD has been described3,4. An increased prevalence of autism-like personality traits is found in unaffected relatives of ASD children, suggesting a genetic liability of a broader autism phenotype (BAP)5. The BAP in parents of autistic children can be assessed by the Social Responsiveness Scale (SRS)6 and Broad Autism Phenotype Questionnaire (BAPQ)7 reports. The SRS is 65-item questionnaire to identify sub-clinical social impairments and interpersonal behaviour in individuals. The BAPQ is a 36-item questionnaire measures social aloofness, rigid personality, and pragmatic language deficits in both parents and children.

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Cardiovascular disease (CVD), particularly coronary heart disease (CHD) and stroke, are the leading cause of morbidity and mortality worldwide. The common forms of CVD have a complex aetiology in which interactions between multiple genetic and environmental factors play an important roles. The incidence rates of these diseases are increasing in developing countries as a result of the modification of lifestyles and increased prevalence of cardiovascular risk factors. Many independent cardiovascular risk factors could be modifiable, in contrast to the genetic risk factors. However, the associated risk of the genetic factors can be prevented if early identified, making genetic studies a priority in cardiovascular genetics research.

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The intestinal tract is exposed to a large variety of antigens such as food proteins, commensal bacteria and pathogens and contains one of the largest arms of the immune system. The intestinal immune system has to discriminate between harmless and harmful antigens, inducing tolerance to harmless antigens and active immunity towards pathogens and other harmful materials. Dendritic cells (DC) in the mucosal lamina propria (LP) are central to this process, as they sample bacteria from the local environment and constitutively migrate to the draining mesenteric lymph nodes (MLN), where they present antigen to naïve T cells in order to direct an appropriate immune response. Despite their crucial role, understanding the function and phenotype of LP DC has been hampered by the fact that they share phenotypic markers with macrophages (mφ), which are the dominant population of mononuclear phagocyte (MP) in the LP. Recent work in our own and other laboratories has established gating strategies and phenotyping panels that allow precise discrimination between intestinal DC and mφ using the mφ specific markers CD64 and F4/80. In this way four bona fide DC subsets with distinct functions have been identified in adult LP based on their expression of CD11b and CD103 and a major aim of my project was to understand how these subsets might develop in the neonatal intestine. At the beginning of my PhD, the laboratory had used these new methods to show that signal regulatory protein α (SIRPα), an inhibitory receptor expressed by myeloid cells, was expressed by mφ and most DC in the intestine, except for those expressing CD103 alone. In addition, mice carrying a non-signalling mutation in SIRPα (SIRPα mt) had a selective reduction in CD103+CD11b+ DC, a subset which is unique to the intestinal LP. This was the basis for the initial experiments of my project, described in Chapter 3, where I investigated if the phenotype in SIRPα mt mice was intrinsic to haematopoietic cells or not. To explore this, I generated bone marrow (BM) chimeric mice by reconstituting irradiated WT mice with SIRPα mt BM, or SIRPα mt animals with WT BM. These experiments suggested that the defect in CD103+CD11b+ DC was not replicated in DC derived from BM of SIRPα origin. However as this seemed inconsistent with other data, I considered the possibility that 18 the phenotype may have been lost with age, as the BM chimeric mice were considerably older than those used in the original studies of SIRPα function. However a comparison of DC subsets in the intestine of WT and SIRPα mt mice as they aged provided no conclusive evidence to support this idea. As these experiments did show age-dependent effects on DC subsets, in Chapter 4, I went on to investigate how the DC populations appeared in the intestine and other tissues in the neonatal period. These experiments showed there were few CD103+CD11b+ DC present in the LP and migratory DC compartment of the MLN in the neonate and that as this population gradually increased in proportion with age, there was a reciprocal decrease in the relative proportion of CD103-CD11b+ DC. Interestingly, most of the changes in DC numbers in the intestine were found during the second or third week of life when the weaning process began. To validate my findings that there were few CD103+CD11b+ DC in the neonate and that this was not merely an absence of CD103 upregulation, I examined the expression of CD101 and Trem-1, markers that other work in the laboratory had suggested were specific to the CD103+CD11b+ DC lineage. My work showed that CD101 and Trem-1 were co- expressed by most CD103+CD11b+ DC in small intestine (SI) LP, as well as a small subset of CD103-CD11b+ DC in this tissue. Interestingly, Trem-1 was highly specific to the SI LP and migratory DC in the MLN, but absent from the colon and other tissues. CD101 expression was also only found on CD11b+ DC, but showed a less restricted pattern of distribution, being found in several tissues as well as the SI LP. The relative timing of their development suggested there might be a relationship between CD103+CD11b+ and CD103-CD11b+ DC and this was supported by microarray analysis. I hypothesised that the CD103-CD11b+ DC that co-expressed CD101 and Trem-1 may be the cells that developed into CD103+CD11b+ DC. To investigate this I analysed how CD101 and Trem-1 expression changed with age amongst the DC subsets in SI LP, colonic LP (CLP) and MLN. The proportion of CD101+Trem-1+ cells increased amongst CD103+CD11b+ DC in the SI LP and MLN with age, while amongst CD103+CD11b+ DC in the CLP this decreased. This was not the same in CD103-CD11b+ DC, where CD101 and Trem-1 expression was more varied with age in all tissues. CD101 and Trem-1 were not expressed to any great extent on CD103+CD11b- or CD103-CD11b- DC. The phenotypic development of the 19 intestinal DC subsets was paralleled by the gradual upregulation of CD103 expression, while the production of retinoic acid (RA), as assessed by the AldefluorTM assay, was low early in life and did not attain adult levels until after weaning. Thus DC in the neonatal intestine take some time to acquire the adult pattern of phenotypic subsets and are functionally immature compared with their adult counterparts. In Chapter 5, I used CD101 and Trem-1 to explore the ontogeny of intestinal DC subsets in CCR2-/- and SIRPα mt mice, both of which have selective defects in one particular group of DC. The selective defect seen amongst CD103+CD11b+ DC in adult SIRPα mt mice was more profound in mice at D7 and D14 of age, indicating that it may be intrinsic to this population and not highly dependent on environmental factors that change after birth. The expression of CD101 and Trem-1 by both CD103+CD11b+ and CD103-CD11b+ DC was reduced in SIRPα mt mice, again indicating that this entire lineage was affected by the lack of SIRPα signalling. However there was also a generalised defect in the numbers of all DC subsets in many tissues from early in life, suggesting there was compromised development, recruitment or survival of DC in the absence of SIRPα signalling. In contrast to the findings in SIRPα mt mice, more CD103+CD11b+ DC co-expressed CD101 and Trem-1 in CCR2-/- mice, while there were no differences in the expression of these molecules amongst CD103-CD11b+ DC. This may suggest that CCR2+ CD103-CD11b+ DC are not the cells that express CD101 and Trem-1 that are predicted to be the direct precursors of CD103+CD11b+ DC. I also examined the expression of DC growth factor receptors on DC subsets from mice of different ages, but no clear age or subset- related patterns of the expression of mRNA for Csf2ra, Irf4, Tgfbr1 and Rara could be observed. Next, I investigated whether Trem-1 played any role in DC development. Preliminary experiments in Trem-1-/- mice show no differences between any of the DC subsets, nor were there any selective effects on individual subsets when DC development from Trem-1-/- KO and WT BM was compared in competitive chimeras. However these experiments were difficult to interpret due to viability problems and because I found an unexpected defect in the ability of Trem-1-/- BM to generate all DC, irrespective of whether they expressed Trem-1 or not. 20 The final experiments I carried out were to examine the role of the microbiota in driving the differentiation of intestinal DC subsets, based on the hypothesis that this could be one of the environmental factors that might influence events in the developing intestine. To this end I performed experiments in both antibiotic treated and germ free adult mice, both of which showed no significant phenotypic differences amongst any of the DC subsets. However the study of germ free mice was compromised by recent contamination of the colony and may not be the conclusive answer. Together the data in this thesis have shown that the population of CD103+CD11b+ DC, which is unique to the intestine, is not present at birth. These cells gradually increase in frequency over time and as this occurs there is a reciprocal decrease in the frequency of CD103-CD11b+ DC. Along with other results, this leads to the idea that there may be a linear developmental pathway from CD103-CD11b+ DC to CD103+CD11b+ DC that is driven by non-microbial factors that are located preferentially in the small intestine. My project indicates that markers such as CD101 and Trem-1 may assist the dissection of this process and highlights the importance of the neonatal period for these events.

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Chronic kidney disease (CKD) is associated with increased cardiovascular risk in comparison with the general population. This can be observed even in the early stages of CKD, and rises in proportion to the degree of renal impairment. Not only is cardiovascular disease (CVD) more prevalent in CKD, but its nature differs too, with an excess of morbidity and mortality associated with congestive cardiac failure, arrhythmia and sudden death, as well as the accelerated atherosclerosis which is also observed. Conventional cardiovascular risk factors such as hypertension, dyslipidaemia, obesity, glycaemia and smoking, are highly prevalent amongst patients with CKD, although in many of these examples the interaction between risk factor and disease differs from that which exists in normal renal function. Nevertheless, the extent of CVD cannot be fully explained by these conventional risk factors, and non-conventional factors specific to CKD are now recognised to contribute to the burden of CVD. Oxidative stress is a state characterised by excessive production of reactive oxygen species (ROS) and other radical species, a reduction in the capacity of antioxidant systems, and disturbance in normal redox homeostasis with depletion of protective vascular signalling molecules such as nitric oxide (NO). This results in oxidative damage to macromolecules such as lipids, proteins and DNA which can alter their functionality. Moreover, many enzymes are sensitive to redox regulation such that oxidative modification to cysteine thiol groups results in activation of signalling cascades which result in adverse cardiovascular effects such as vascular and endothelial dysfunction. Endothelial dysfunction and oxidative stress are present in association with many conventional cardiovascular risk factors, and can be observed even prior to the development of overt, clinical, vascular pathology, suggesting that these phenomena represent the earliest stages of CVD. In the presence of CKD, there is increased ROS production due to upregulated NADPH oxidase (NOX), increase in a circulating asymmetric dimethylarginine (ADMA), uncoupling of endothelial nitric oxide synthase (eNOS) as well as other mechanisms. There is also depletion in exogenous antioxidants such as ascorbic acid and tocopherol, and a reduction in activity of endogenous antioxidant systems regulated by the master gene regulator Nrf-2. In previous studies, circulating markers of oxidative stress have been shown to be increased in CKD, together with a reduction in endothelial function in a stepwise fashion relating to the severity of renal impairment. Not only is CVD linked to oxidative stress, but the progression of CKD itself is also in part dependent on redox sensitive mechanisms. For example, administration of the ROS scavenger tempol attenuates renal injury and reduces renal fibrosis seen on biopsy in a mouse model of CKD, whilst conversely, supplementation with the NOS inhibitor L-NAME causes proteinuria and renal impairment. Previous human studies examining the effect of antioxidant administration on vascular and renal function have been conflicting however. The work contained in this thesis therefore examines the effect of antioxidant administration on vascular and endothelial function in CKD. Firstly, 30 patients with CKD stages 3 – 5, and 20 matched hypertensive controls were recruited. Participants with CKD had lower ascorbic acid, higher TAP and ADMA, together with higher augmentation index and pulse wave velocity. There was no difference in baseline flow mediated dilatation (FMD) between groups. Intravenous ascorbic acid increased TAP and O2-, and reduced central BP and augmentation index in both groups, and lowered ADMA in the CKD group only. No effect on FMD was observed. The effects of ascorbic acid on kidney function was then investigated, however this was hindered by the inherent drawbacks of existing methods of non-invasively measuring kidney function. Arterial spin labelling MRI is an emerging imaging technique which allows measurement of renal perfusion without administration of an exogenous contrast agent. The technique relies upon application of an inversion pulse to blood within the vasculature proximal to the kidneys, which magnetically labels protons allowing measurement upon transit to the kidney. At the outset of this project local experience using ASL MRI was limited and there ensued a prolonged pre-clinical phase of testing with the aim of optimising imaging strategy. A study was then designed to investigate the repeatability of ASL MRI in a group of 12 healthy volunteers with normal renal function. The measured T1 longitudinal relaxation times and ASL MRI perfusion values were in keeping with those found in the literature; T1 time was 1376 ms in the cortex and 1491 ms in the whole kidney ROI, whilst perfusion was 321 mL/min/100g in the cortex, and 228 mL/min/100g in the whole kidney ROI. There was good reproducibility demonstrated on Bland Altman analysis, with a CVws was 9.2% for cortical perfusion and 7.1% for whole kidney perfusion. Subsequently, in a study of 17 patients with CKD and 24 healthy volunteers, the effects of ascorbic acid on renal perfusion was investigated. Although no change in renal perfusion was found following ascorbic acid, it was found that ASL MRI demonstrated significant differences between those with normal renal function and participants with CKD stages 3 – 5, with increased cortical and whole kidney T1, and reduced cortical and whole kidney perfusion. Interestingly, absolute perfusion showed a weak but significant correlation with progression of kidney disease over the preceding year. Ascorbic acid was therefore shown to have a significant effect on vascular biology both in CKD and in those with normal renal function, and to reduce ADMA only in patients with CKD. ASL MRI has shown promise as a non-invasive investigation of renal function and as a biomarker to identify individuals at high risk of progressive renal impairment.

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A produção e qualidade do leite são influenciadas por factores ambientais como a nutrição, factores genéticos como a raça, e factores fisiológicos como a idade a idade ao parto ou o número de ordenhas diárias. Este trabalho teve por objectivo estimar factores de correcção para os efeitos ambientais que influenciam a quantidade e qualidade do leite com vista ao melhoramento genético dos animais. Para isso, foram utilizados os registos de 23897 contrastes leiteiros de vacas de raça Frísia, no período de 6 anos, recolhidos a partir dos dados da ANABLE. De acordo com os resultados, obtidos através do método dos quadrados mínimos, observa-se que para a produção de leite, gordura e proteína, todos os efeitos fixos de variação são significativos nas três características produtivas estudadas, pelo que se conclui que há interacção entre a idade da vaca ao parto e a produção e qualidade do leite, assim como, a época do ano em que ocorre o parto e o número de ordenhas diárias a que o animal está sujeito. ABSTRACT; Cow production and milk quality are influenced by environmental factors such as nutrition, by genetic factors as breed and physiological factors as age at calving or milking frequency. This study aimed to estimate correction parameters for environmental factors with influence on milk production and quality embodying genetic improvement. For this propose, a data base was used with information related to 23987 milk tests collected from official milk recording program. According to the results, where the at least square procedure was adopted, it shows that all the fixed effects of variation significantly affect the productive performances, so it can be concluded that there is a significant interaction between milking frequency, age at calving and season when it occurs, and milk production and quality.

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The Federal Institution for Education, Science and Technology, in its historical path, has been living different changes. The transformations occurred along the way have been determined by coercive forces from the institutional environment, which has became more and more broad and complex throughout the time, obtaining diverse characteristics and new elements such as non institutional factors1 which started to contribute with the other changes. In this context, this work aims to study the isomorphic practices of the managers in the institutional changes process of the IFRN in 1998 and 2008, as of a theoretical coevolutionary perspective (CHILD; RODRIGUES; LEWIN; CARROL; VOLBERDA, 2003). This theory brings a new point of view for the organization analysis to the organizational studies, since it offers a non deterministic and non linear lection of the evolution process, which means, a coevolution. Thus, the organizations and their institutional and non institutional environment auto evolve, auto organize and auto reproduce. Therefore, the institutional and non institutional factors of the macro environment keep a continuous interdependence relationship with the organizations. For the means of this study, it is important to understand that is impossible to comprehend the object, the isomorphic practices, without considering that the previous institutional changes and its evolutions, its continuations and discontinuations, important in the coevolution process. As such, to call upon the institutional historical track is a fundamental aspect to materialize this study, for the recursive movement is indeed present in the coevolution. Another important point to make this research effective is that it is not possible to abdicate from the hologramatic view2 of this study, which considers the object, the isomorphic practices, part of the whole and this whole is also in the parts, therefore it is impossible to comprehend the object of study outside the context where it belongs. With this, as of the objective previously proposed, it is necessary to describe the characteristics of coevolution of the institutional changes related in 1998 and 2008; analyze the dynamic of the isomorphic mechanisms in its respective institutional change process; and describe the lessons learned which the isomorphic practices left to the IFRN, regarding its benefits and difficulties. All these transformations happened through coercive forces3 of the institutional environment. As of the Nineties, these forces became stronger, the environment became broader and more complex, with the emergency of new environmental factors. This study proposed to study the managing process and its practices, related to the micro environment, although it is required to articulate these actions, the demands and requirements from the macro environment. To make this research effective, semi structured interviews have been conducted with the managers who participated in both institutional change processes. In the results analysis, it has been possible to verify the particularity of each change, the one from 1998 with a strong normative action of the managers against coercive forces from the government for the search of recognition and the institutional legitimation and the one in 2008, which has been characterized by the normative action by managers in agreement with the coercive forces from the government, in favor of the government policy for the technological professional education. However, the results analysis it is possible to notice the evidence of a belonging feeling from the interviewed managers

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Contexte et objectifs. Le contrôle de soi serait, selon Gottfredson et Hirschi (1990), le meilleur prédicteur de la délinquance. Il serait déterminé, selon les auteurs, exclusivement par les facteurs environnementaux (compétences parentales, surveillance et punition) et ce, avant l'âge de sept ans. Il ne serait pas question des facteurs génétiques dans l'étiologie du contrôle de soi. Or, plusieurs études récentes menées à l'adolescence et à l'âge adulte avancent que le contrôle de soi serait d'origine partiellement génétique. Deux objectifs seront poursuivis. D'abord, considérant que le contrôle de soi, tel que décrit par Gottfredson et Hirschi (1990), n'ait jamais été étudié spécifiquement à la petite enfance, il a été nécessaire d'opérationnaliser le construit à la petite enfance à partir des informations existantes sur le contrôle de soi. Ensuite, il s'agira d'estimer l’influence relative des facteurs génétiques et environnementaux sur le contrôle de soi à 18, 30 et 48 mois. Méthodologie. En tout, 672 familles de jumeaux monozygotes ou dizygotes de la grande région métropolitaine de Montréal ont pris part à l'Étude des jumeaux nouveau-nés du Québec. Les items utilisés proviennent du Child Behavior Checklist (Achenbach, 1994) et ont été obtenus via les parents des jumeaux. La zygotie a été évaluée à l’aide du Zygosity Questionnaire for Young Twins (Goldsmith, 1991) et le sexe a été déterminé par les assistants de recherché. Trois temps de mesures furent étudiés : 18 mois (n = 664), 30 mois (n = 617) et 48 mois (n = 531). Résultats. Les résultats des analyses factorielles confirmatoires suggèrent par le biais des estimés qu'il soit possible de générer un facteur du contrôle de soi à la petite enfance à partir des indicateurs sélectionnés et que ceux-ci se regroupent sous l'égide d'un seul facteur. Les résultats concernant l’étiologie montrent que les différences individuelles observées seraient, majoritairement influencées par les facteurs génétiques (additifs ou de dominance) suivis par les environnements uniques. Conclusion. Les résultats suggèrent que les facteurs génétiques jouent un rôle important dans l’étiologie des différences individuelles dans le contrôle de soi tôt dans le développement alors que les environnements communs ne seraient pas impliqués. Les résultats sont compatibles avec les études menées à l'adolescence et à l'âge adulte et sont en contradiction avec les postulats de Gottfredson et Hirschi (1990).

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Contexte et objectifs. Le contrôle de soi serait, selon Gottfredson et Hirschi (1990), le meilleur prédicteur de la délinquance. Il serait déterminé, selon les auteurs, exclusivement par les facteurs environnementaux (compétences parentales, surveillance et punition) et ce, avant l'âge de sept ans. Il ne serait pas question des facteurs génétiques dans l'étiologie du contrôle de soi. Or, plusieurs études récentes menées à l'adolescence et à l'âge adulte avancent que le contrôle de soi serait d'origine partiellement génétique. Deux objectifs seront poursuivis. D'abord, considérant que le contrôle de soi, tel que décrit par Gottfredson et Hirschi (1990), n'ait jamais été étudié spécifiquement à la petite enfance, il a été nécessaire d'opérationnaliser le construit à la petite enfance à partir des informations existantes sur le contrôle de soi. Ensuite, il s'agira d'estimer l’influence relative des facteurs génétiques et environnementaux sur le contrôle de soi à 18, 30 et 48 mois. Méthodologie. En tout, 672 familles de jumeaux monozygotes ou dizygotes de la grande région métropolitaine de Montréal ont pris part à l'Étude des jumeaux nouveau-nés du Québec. Les items utilisés proviennent du Child Behavior Checklist (Achenbach, 1994) et ont été obtenus via les parents des jumeaux. La zygotie a été évaluée à l’aide du Zygosity Questionnaire for Young Twins (Goldsmith, 1991) et le sexe a été déterminé par les assistants de recherché. Trois temps de mesures furent étudiés : 18 mois (n = 664), 30 mois (n = 617) et 48 mois (n = 531). Résultats. Les résultats des analyses factorielles confirmatoires suggèrent par le biais des estimés qu'il soit possible de générer un facteur du contrôle de soi à la petite enfance à partir des indicateurs sélectionnés et que ceux-ci se regroupent sous l'égide d'un seul facteur. Les résultats concernant l’étiologie montrent que les différences individuelles observées seraient, majoritairement influencées par les facteurs génétiques (additifs ou de dominance) suivis par les environnements uniques. Conclusion. Les résultats suggèrent que les facteurs génétiques jouent un rôle important dans l’étiologie des différences individuelles dans le contrôle de soi tôt dans le développement alors que les environnements communs ne seraient pas impliqués. Les résultats sont compatibles avec les études menées à l'adolescence et à l'âge adulte et sont en contradiction avec les postulats de Gottfredson et Hirschi (1990).