153 resultados para fragmentation processes
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AIM: Phylogenetic diversity patterns are increasingly being used to better understand the role of ecological and evolutionary processes in community assembly. Here, we quantify how these patterns are influenced by scale choices in terms of spatial and environmental extent and organismic scales. LOCATION: European Alps. METHODS: We applied 42 sampling strategies differing in their combination of focal scales. For each resulting sub-dataset, we estimated the phylogenetic diversity of the species pools, phylogenetic α-diversities of local communities, and statistics commonly used together with null models in order to infer non-random diversity patterns (i.e. phylogenetic clustering versus over-dispersion). Finally, we studied the effects of scale choices on these measures using regression analyses. RESULTS: Scale choices were decisive for revealing signals in diversity patterns. Notably, changes in focal scales sometimes reversed a pattern of over-dispersion into clustering. Organismic scale had a stronger effect than spatial and environmental extent. However, we did not find general rules for the direction of change from over-dispersion to clustering with changing scales. Importantly, these scale issues had only a weak influence when focusing on regional diversity patterns that change along abiotic gradients. MAIN CONCLUSIONS: Our results call for caution when combining phylogenetic data with distributional data to study how and why communities differ from random expectations of phylogenetic relatedness. These analyses seem to be robust when the focus is on relating community diversity patterns to variation in habitat conditions, such as abiotic gradients. However, if the focus is on identifying relevant assembly rules for local communities, the uncertainty arising from a certain scale choice can be immense. In the latter case, it becomes necessary to test whether emerging patterns are robust to alternative scale choices.
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Abstract The production of various reactive oxidant species in excess of endogenous antioxidant defense mechanisms promotes the development of a state of oxidative stress, with significant biological consequences. In recent years, evidence has emerged that oxidative stress plays a crucial role in the development and perpetuation of inflammation, and thus contributes to the pathophysiology of a number of debilitating illnesses, such as cardiovascular diseases, diabetes, cancer, or neurodegenerative processes. Oxidants affect all stages of the inflammatory response, including the release by damaged tissues of molecules acting as endogenous danger signals, their sensing by innate immune receptors from the Toll-like (TLRs) and the NOD-like (NLRs) families, and the activation of signaling pathways initiating the adaptive cellular response to such signals. In this article, after summarizing the basic aspects of redox biology and inflammation, we review in detail the current knowledge on the fundamental connections between oxidative stress and inflammatory processes, with a special emphasis on the danger molecule high-mobility group box-1, the TLRs, the NLRP-3 receptor, and the inflammasome, as well as the transcription factor nuclear factor-κB.
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The plutonic rocks of the Basal Complex of La Gomera, Canary Islands, Spain, were studied by means of major and trace element contents and by H-O-Sr-Nd isotope compositions in order to distinguish primary magmatic characteristics and late-stage alteration products. Deciphering the effects of alteration allowed us to determine primary, plume-related compositions that indicated D- and (18)O-depletion relative to normal upper mantle, supporting the conclusions of earlier studies on the plutonic rocks of Fuerteventura and La Palma. Late-stage alteration took place during the formation of the intrusive series induced by interaction with meteoric water. Inferred isotopic compositions of the meteoric water indicate that the water infiltrated into the rock edifice at a height of about 1500 m above sea level, suggesting the existence of a subaerial volcano which was active during the intrusive activity and that it has been either distroyed or remain buried by later volcanic and landslide events.
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Based on the case of reforms aimed at integrating the provision of income protection and employment services for jobless people in Europe, this thesis seeks to understand the reasons which may prompt governments to engage in large-scale organisational reforms. Over the last 20 years, several European countries have indeed radically redesigned the organisational structure of their welfare state by merging or bundling existing front-line offices in charge of benefit payment and employment services together into 'one-stop' agencies. Whereas in academic and political debates, these reforms are generally presented as a necessary and rational response to the problems and inconsistencies induced by fragmentation in a context of the reorientation of welfare states towards labour market activation, this thesis shows that the agenda setting of these reforms is in fact the result of multidimensional political dynamics. More specifically, the main argument of this thesis is that these reforms are best understood not so such from the problems induced by organisational compartmentalism, whose political recognition is often controversial, but from the various goals that governments may simultaneously achieve by means of their adoption. This argument is tested by comparing agenda-setting processes of large-scale reforms of coordination in the United Kingdom (Jobcentre Plus), Germany (Hartz IV reform) and Denmark (2005 Jobcentre reform), and contrasting them with the Swiss case where the government has so far rejected any coordination initiative involving organisational redesign. This comparison brings to light the importance, for the rise of organisational reforms, of the possibility to couple them with the following three goals: first, goals related to the strengthening of activation policies; second, institutional goals seeking to redefine the balance of responsibilities between the central state and non-state actors, and finally electoral goals for governments eager to maintain political credibility. The decisive role of electoral goals in the three countries suggests that these reforms are less bound by partisan politics than by the particular pressures facing governments arrived in office after long periods in opposition.
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The discovery of exhumed continental mantle and hyper-extended crust in present-day magma-poor rifted margins is at the origin of a paradigm shift within the research field of deep-water rifted margins. It opened new questions about the strain history of rifted margins and the nature and composition of sedimentary, crustal and mantle rocks in rifted margins. Thanks to the benefit of more than one century of work in the Alps and access to world-class outcrops preserving the primary relationships between sediments and crustal and mantle rocks from the fossil Alpine Tethys margins, it is possible to link the subsidence history and syn-rift sedimentary evolution with the strain distribution observed in the crust and mantle rocks exposed in the distal rifted margins. In this paper, we will focus on the transition from early to late rifting that is associated with considerable crustal thinning and a reorganization of the rift system. Crustal thinning is at the origin of a major change in the style of deformation from high-angle to low-angle normal faulting which controls basin-architecture, sedimentary sources and processes and the nature of basement rocks exhumed along the detachment faults in the distal margin. Stratigraphic and isotopic ages indicate that this major change occurred in late Sinemurian time, involving a shift of the syn-rift sedimentation toward the distal domain associated with a major reorganization of the crustal structure with exhumation of lower and middle crust. These changes may be triggered by mantle processes, as indicated by the infiltration of MOR-type magmas in the lithospheric mantle, and the uplift of the Brianconnais domain. Thinning and exhumation of the crust and lithosphere also resulted in the creation of new paleogeographic domains, the Proto Valais and Liguria-Piemonte domains. These basins show a complex, 3D temporal and spatial evolution that might have evolved, at least in the case of the Liguria-Piemonte basin, in the formation of an embryonic oceanic crust. The re-interpretation of the rift evolution and the architecture of the distal rifted margins in the Alps have important implications for the understanding of rifted margins worldwide, but also for the paleogeographic reconstruction of the Alpine domain and its subsequent Alpine compressional overprint.
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The Monte Perdido thrust fault (southern Pyrenees) consists of a 6-m-thick interval of intensely deformed clay-bearing rocks. The fault zone is affected by a pervasive pressure solution seam and numerous shear surfaces. Calcite extensional-shear veins are present along the shear surfaces. The angular relationships between the two structures indicate that shear surfaces developed at a high angle (70°) to the local principal maximum stress axis r1. Two main stages of deformation are present. The first stage corresponds to the development of calcite shear veins by a combination of shear surface reactivation and extensional mode I rupture. The second stage of deformation corresponds to chlorite precipitation along the previously reactivated shear surfaces. The pore fluid factor k computed for the two deformation episodes indicates high fluid pressures during the Monte Perdido thrust activity. During the first stage of deformation, the reactivation of the shear surface was facilitated by a suprahydrostatic fluid pressure with a pore fluid factor kv equal to 0.89. For the second stage, the fluid pressure remained still high (with a k value ranging between 0.77 and 0.84) even with the presence of weak chlorite along the shear surfaces. Furthermore, evidence of hydrostatic fluid pressure during calcite cement precipitation supports that incremental shear surface reactivations are correlated with cyclic fluid pressure fluctuations consis- tent with a fault-valve model.
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Understanding the function of variation in sleep requires studies in the natural ecological conditions in which sleep evolved. Sleep has an impact on individual performance and hence may integrate the costs and benefits of investing in processes that are sensitive to sleep, such as immunity or coping with stress. Because dark and pale melanic animals differentially regulate energy homeostasis, immunity and stress hormone levels, the amount and/or organization of sleep may covary with melanin-based colour. We show here that wild, cross-fostered nestling barn owls (Tyto alba) born from mothers displaying more black spots had shorter non-REM (rapid eye movement) sleep bouts, a shorter latency until the occurrence of REM sleep after a bout of wakefulness and more wakefulness bouts. In male nestlings, the same sleep traits also correlated with their own level of spotting. Because heavily spotted male nestlings and the offspring of heavily spotted biological mothers switched sleep-wakefulness states more frequently, we propose the hypothesis that they could be also behaviourally more vigilant. Accordingly, nestlings from mothers displaying many black spots looked more often towards the nest entrance where their parents bring food and towards their sibling against whom they compete. Owlets from heavily spotted mothers might invest more in vigilance, thereby possibly increasing associated costs due to sleep fragmentation. We conclude that different strategies of the regulation of brain activity have evolved and are correlated with melanin-based coloration.
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PPARalpha and PPARbeta are expressed in the mouse epidermis during fetal development, but their expression progressively disappears after birth. However, the expression of PPARbeta is reactivated in adult mice upon proliferative stimuli, such as cutaneous injury. We show here that PPARbeta protects keratinocytes from growth factor deprivation, anoikis and TNF-alpha-induced apoptosis, by modulating both early and late apoptotic events via the Akt1 signaling pathway and DNA fragmentation, respectively. The control mechanisms involve direct transcriptional upregulation of ILK, PDK1, and ICAD-L. In accordance with the anti-apoptotic role of PPARbeta observed in vitro, the balance between proliferation and apoptosis is altered in the epidermis of wounded PPARbeta mutant mice, with increased keratinocyte proliferation and apoptosis. In addition, primary keratinocytes deleted for PPARbeta show defects in both cell-matrix and cell-cell contacts, and impaired cell migration. Together, these results suggest that the delayed wound closure observed in PPARbeta mutant mice involves the alteration of several key processes. Finally, comparison of PPARbeta and Akt1 knock-out mice reveals many similarities, and suggests that the ability of PPARbeta to modulate the Akt1 pathway has significant impact during skin wound healing.
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Résumé La responsabilité d'un expert chargé d'apprécier la capacité érectile d'un prévenu est importante, car la peine infligée par le tribunal peut dépendre de ses conclusions. Sa tâche est en plus ardue car les procédés d'investigations de la fonction érectile ont tous des limites. Malgré toutes ces limites qui sont décrites dans cet article, l'expert peut aider à la recherche de la vérité comme les auteurs le démontrent. Summary The responsability of the expert in charge to appreciate the erectile capacity of an accused is considerable, as the sentence inflicted by the Tribunal could depend directly on his conclusions. His duty is harder as all the investigation procedures of the erectile functions have limits. Despite these limits, described in this article, the expert can help to discover the truth, as demonstrated by the authors.
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Clarification-Oriented Psychotherapy (COP), an integrative treatment form with a basis in process-experiential psychotherapy, is particularly relevant for clients with Personality Disorders (PDs). We argue here that two related core therapeutic COP principles, "dual action regulation" and "interactional games" have consequences for symptom severity and therapeutic outcome for clients with PDs. A high quality COP clarification process requires that client's interactional games may be quickly assessed and treated in all (preferably early) therapy sessions. These processes can be observed and measured using the observer-rated Bochum Process and Relationship Rating Scales (BPRRS) which measure both clients' and therapists' contributions to the quality of the clarification processes engaged in therapy. This measure has been successfully applied to COP-therapies, but not, as yet, to therapies other than experiential, nor to specific client populations such as borderline personality disorder. The present study is a first attempt to evaluate the application of COP processes to other therapies and populations. We measured action regulation and interactional games using the BPRRS during intake sessions of a 10-session psychodynamic treatment of borderline personality disorder for a total of N = 30 clients and N = 8 therapists. Significant relationships were found between the client's degree of interactional games and both pretherapy symptom level and symptom change across therapy. These results are discussed in the context of Clarification-Oriented Psychotherapy, and more generally Person-Centered and Process-Experiential Psychotherapies. The potential relevance of the findings for psychodynamic psychotherapists are explored as well as the potential usefulness of taking into account a detailed analysis of interactional games for the training of psychotherapists working with any model of therapy working with clients presenting with BPD.
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Collectively, research aimed to understand the regeneration of certain tissues has unveiled the existence of common key regulators. Knockout studies of the murine Nuclear Factor I-C (NFI-C) transcription factor revealed a misregulation of growth factor signaling, in particular that of transforming growth factor ß-1 (TGF-ßl), which led to alterations of skin wound healing and the growth of its appendages, suggesting it may be a general regulator of regenerative processes. We sought to investigate this further by determining whether NFI-C played a role in liver regeneration. Liver regeneration following two-thirds removal of the liver by partial hepatectomy (PH) is a well-established regenerative model whereby changes elicited in hepatocytes following injury lead to a rapid, phased proliferation. However, mechanisms controlling the action of liver proliferative factors such as transforming growth factor-ßl (TGF-ß1) and plasminogen activator inhibitor-1 (PAI-1) remain largely unknown. We show that the absence of NFI-C impaired hepatocyte proliferation due to an overexpression of PAI-1 and the subsequent suppression of urokinase plasminogen (uPA) activity and hepatocyte growth factor (HGF) signaling, a potent hepatocyte mitogen. This indicated that NFI-C first acts to promote hepatocyte proliferation at the onset of liver regeneration in wildtype mice. The subsequent transient down regulation of NFI-C, as can be explained by a self- regulatory feedback loop with TGF-ßl, may limit the number of hepatocytes entering the first wave of cell division and/or prevent late initiations of mitosis. Overall, we conclude that NFI-C acts as a regulator of the phased hepatocyte proliferation during liver regeneration. Taken together with NFI-C's actions in other in vivo models of (re)generation, it is plausible that NFI-C may be a general regulator of regenerative processes. - L'ensemble des recherches visant à comprendre la régénération de certains tissus a permis de mettre en évidence l'existence de régulateurs-clés communs. L'étude des souris, dépourvues du gène codant pour le facteur de transcription NFI-C (Nuclear Factor I-C), a montré des dérèglements dans la signalisation de certains facteurs croissance, en particulier du TGF-ßl (transforming growth factor-ßl), ce qui conduit à des altérations de la cicatrisation de la peau et de la croissance des poils et des dents chez ces souris, suggérant que NFI-C pourrait être un régulateur général du processus de régénération. Nous avons cherché à approfondir cette question en déterminant si NFI-C joue un rôle dans la régénération du foie. La régénération du foie, induite par une hépatectomie partielle correspondant à l'ablation des deux-tiers du foie, constitue un modèle de régénération bien établi dans lequel la lésion induite conduit à la prolifération rapide des hépatocytes de façon synchronisée. Cependant, les mécanismes contrôlant l'action de facteurs de prolifération du foie, comme le facteur de croissance TGF-ßl et l'inhibiteur de l'activateur du plasminogène PAI-1 (plasminogen activator inhibitor-1), restent encore très méconnus. Nous avons pu montrer que l'absence de NFI-C affecte la prolifération des hépatocytes, occasionnée par la surexpression de PAI-1 et par la subséquente suppression de l'activité de la protéine uPA (urokinase plasminogen) et de la signalisation du facteur de croissance des hépatocytes HGF (hepatocyte growth factor), un mitogène puissant des hépatocytes. Cela indique que NFI-C agit en premier lieu pour promouvoir la prolifération des hépatocytes au début de la régénération du foie chez les souris de type sauvage. La subséquente baisse transitoire de NFI-C, pouvant s'expliquer par une boucle rétroactive d'autorégulation avec le facteur TGF-ßl, pourrait limiter le nombre d'hépatocytes qui entrent dans la première vague de division cellulaire et/ou inhiber l'initiation de la mitose tardive. L'ensemble de ces résultats nous a permis de conclure que NFI-C agit comme un régulateur de la prolifération des hépatocytes synchrones au cours de la régénération du foie.