NCube/papyrus huggingface dataset:
Peinture de lumière incidente dans des scènes 3D

Lighting design is usually a task that is done manually, where the artists must manipulate the parameters of several light sources to obtain the desired result. This task is difficult because it is not intuitive. Some systems already exist that enable a user to paint light directly on objects in a scene to position or alter light sources. Unfortunately, these systems have some limitations such that they only consider local lighting, or the camera must be fixed, etc. Either way, this limitates the accuracy or the versatility of these systems. Global illumination is important because it adds a lot of realism to a scene by capturing all the light interreflections on the surfaces. This means that light sources can influence surfaces even if they are not directly exposed.  In this M. Sc. thesis, we study a subset of the lighting design problem: the selection and alteration of the intensity of light sources. We present two different systems to design lighting on objects in 3D scenes. The user paints light intentions directly on the objects to alter the surface illumination. From these paint strokes, the systems find the light sources and alter their intensity to obtain as much as possible what the user wants. The novelty of our technique is that global illumination, transparent surfaces and subsurface scattering are all considered, and also that the camera is free to take any position. We also present strategies for selecting and altering the light sources.  The first system uses an environment map as an intermediate representation of the environment surrounding the objects. The second system saves all the information of the environment for each vertex of each object.

Keyphrases: Rendu inverse, Light Design, Inverse Rendering, Global Illumination, Painting Metaphor
Modulation of Oxytocin Receptors in Right Ventricular Hypertrophy

Pulmonary hypertension (PH) is a disease of unknown etiology that ultimately causes failure of right ventricle (RV) with a lethal outcome. PH can be induced in the rat with monocrotaline (MCT), a pyrrolizidine alkaloid from the plant Crotolaria spectabilis that damages the pulmonary artery endothelium leading to thickening of the pulmonary arteries and increased vascular resistance. This subsequently results in RV hypertrophy, inflammation, nitric oxide (NO)-associated coronary endothelial dysfunction and increment of natriuretic peptides (NP) in the circulation.  Objective: We verified hypothesis that the etiopathogenesis of PH involves the oxytocin receptor (OTR) because of its functional association with inflammatory cytokines and release of atrial natriuretic peptide (ANP) and NO. Methods: Male Sprague-Dawley rats weighing 220-250g received a single subcutaneous injection of 60 mg/kg of MCT. Six to 7 weeks (46±1 days) following the injection, rats were sacrificed and gene and protein expression were detected by real-time PCR and western-blot analysis, respectively, in the RV and LV (left ventricle). Results: MCT-treated rats displayed significant increases in RV weight. RV hypertrophy was evident as the ratio of the RV to LV plus septum weight was nearly 77% higher in MCT-treated rats compared to control rats. MCT treatment increased transcripts of ANP (3.7-fold in the LV and 8-fold in RV) and brain NP (2.7-fold in the LV and 10-fold in RV). Transcripts for three NP receptors significantly increased (0.3-2 fold) only in the RV. iNOS (inducible NO synthase) protein expression also increased selectively in the RV. In contrast, the endothelial NOS and neural NOS transcripts heightened (0.5-2 fold) in the LV. Both OTR mRNA and protein were decreased by 50% in the RV, whereas an up-regulation of cytokines IL-1β and IL-6 was observed. Nab1 mRNA, a marker of pathological hypertrophy, increased two-fold in the RV. Conclusion: Increased gene expression of NP in the RV of the MCT-treated rat correlates with upregulation of NP receptor transcripts indicating local NP action in the RV during PH. OTR expression is decreased in the RV possibly by inflammatory cytokines, IL-1 and IL-6 because OTR promoter region contains multiple putative interleukin-response elements. Lowering OTR in RV during pulmonary hypertension can influence cardiac function since OT regulates heart rate and cardiac contractility and is linked with cardioprotective system ANP and NO.   Keywords: pulmonary hypertension, right ventricular hypertrophy, monocrotaline, oxytocin receptor, inflammation, natriuretic peptides.

Keyphrases: Pulmonary hypertension, Right ventricular hypertrophy, Oxytocin receptor, Inflammation, Inflammation, Natriuretic peptides
Joyau du patrimoine mondial et tourisme : l'exemple de St-George, Bermudes

This dissertation presents the case study of the town of St. George, historic capital of Bermuda. Its unique geography, the presence of British colonial architecture and of many military forts allowed its inclusion on the UNESCO world heritage List. This nomination in itself constitutes a recognition of the exceptional universal value of this urban entity. This inscription happens at the exact moment where the local authorities wish to diversify the archipelago’s economy by exploiting cultural and heritage tourism.  The hypothesis of this dissertation is that the town of St. George is, according to the proposition of G.J Ashworth and J.E Tunbridge in their book The tourist-historic city, a «heritage gem », that is, a small community containing a great number of exceptional historic resources shaping the urban morphology, the landscape identity and local policies.  The research, following the introduction of the relevant theoretical framework on world heritage and heritage tourism, demonstrated that the concept of the “tourist-historic city” developed by the same authors can be easily applied to the case of Bermuda if a scale reduction is made. Indeed, we are not presented with a touristic space created by two different sectors of the same city, but by two small neighbouring cities – St. George and Hamilton, the capital – which are the basis of a fragmented tourist-historic city.

Keyphrases: Bermuda, Tourism, Historical center, Heritage, World heritage
La démocratie à l’épreuve du projet : les effets d’un processus de planification concertée à Porto Alegre

It is quite common, when discussing city planning, to call upon the necessity of public participation. However, the means by which the public participates are still mainly left to experimentation and uncertainty. This dissertation questions the institutional design of participation processes in city planning, from the angle of their democratization effects. It will tempt to identify determining aspects of public participation processes in city planning in order to offer, to those who design them, keys to understanding the implications of their choices. The analysis will be based on the study of the day-to-day operations of a collaborative planning process in the Lomba do Pinheiro district of Porto Alegre. It will use a sectioning of process components built from a review of technical books on participation in design Having depicted Porto Alegre’s specific participation and planning culture and how it was constructed, the analysis will, by observing the evolution of the process and its result, describe the process’ effects in terms of impacts on the built environment, on the transformation of social relations, and on the possibility of making conflicts apparent. Conclusions will reveal the significance of informal aspects in the work of facilitators as well as the necessity to put the project at the center of the process in order to establish a common ground. The crucial role placed by the selection of participants will be outlined. Strong doubts will be expressed on the relevance of the transformation of social relation as a goal of collaborative planning.

Keyphrases: Public participation in city planning, Collaborative planning, Institutional design, Porto Alegre, Porto Alegre, Lomba do Pinheiro, Lomba do Pinheiro
Deletion of the RNR4 gene causes hyperresistance to the carcinogen 4-NQO in the yeast model

Genomic stability, critical for life, is controlled by DNA replication and repair.  DNA replication and repair is mediated through many enzymes, one being ribonucleotide reductase (RNR), an enzyme found in both yeast and humans. RNR catalyzes the reaction involved in the formation of deoxyribonucleotides and is responsible for maintaining dNTP pools required for DNA repair and replication. RNR is an α2β2 tetramer consisting of a large (R1, α2) and small subunit (R2, β2). In S. cerevisiae RNR1 and RNR3 encode α2 (R1). RNR catalytic activity depends on its interaction with iron and on the formation of the complex between R1 and R2. All subunits are inducible by DNA damage.  Here we show that cells lacking one subunit, Rnr4, of the RNR complex are sensitive to various DNA damaging agents such as methyl methane sulfonate, bleomycin, hydrogen peroxide, and ultraviolet radiation (UVC 254 nm). In contrast, the mutant is resistant to 4-nitroquinoline-1-oxide (4-NQO), an agent which produces bulky lesions. Consistent with this resistance, the rnr4Δ showed a sharp reduction in 4-NQO-induced mutations as compared to the parent.  We wanted to determine which pathway was able to confer resistance to 4-NQO and thus targeted DNA repair proteins. The repair pathways BER, NER and MMR did not abolish 4-NQO resistance in rnr4Δ. Recombination protein Rad51 (NHEJ) was lethal in an rnr4Δ thus indicating no role in DNA repair and 4-NQO resistance. Deletion of the REV3 gene, encoding a DNA bypass polymerase involved in post replication repair, partially abolished 4-NQO resistance in rnr4Δ. These results suggest that Rev3 and possibly other translesion polymerases (Rev1, Rev7, Rad30) could play a role in the repair of bulky DNA lesions under low levels of dNTPs. DNA repair, a complex mechanism in yeast, involves a vast array of proteins, some yet to be discovered. Our results indicate that there is more than one protein involved in 4-NQO resistance and further investigation is required concerning recombination and post replication repair.

Keyphrases: DNA repair, RNR, 4-NQO resistance, Recombination, Bypass polymerase, RNR, 4-NQO
Action anti-leucémique des inhibiteurs de la méthylation de l’ADN et de la déacétylation des histones

The silencing of tumor suppressor genes (TSG) that normally regulate cells proliferation plays an important role in leukemogenesis. Two major mechanisms are involved in TSG’s silencing: DNA methylation and histones deacetylation. Because those phenomenons are reversible, it makes them interesting therapeutic targets for chemotherapeutic agents. We evaluated the antineoplastic potential of different agents that target those events and we administered them alone or in combination with the goal of improving their efficiency.    5-aza-2’-deoxycytidine (5-Aza-CdR) is a DNA methylation inhibitor that can re-express TSGs that are silenced by methylations. This agent demonstrated its efficacy against hematological malignancies. Therefore, 5-Aza-CdR is used since 2006 in United States of America against myelodysplastic syndrome; but its optimal dose-schedule still needs to be established. Our researches suggest that the dose-schedule of 5-Aza-CdR should be more intensive than what is reported from the literature.    Inhibitors of histones deacetylation (HDACi) also demonstrated some interesting antineoplastic activity. Recently, observations showed that combination of chemotherapeutic agent that targets both DNA methylation and histones deacetylation lead to a synergic reactivation of silenced TSG. This finding allowed us to observe that the co-administration of an HDACi with 5-Aza-CdR improve its antileukemic potential.    Moreover, it is possible to increase the activity of 5-Aza-CdR by preventing its degradation by cytidine (CR) deaminase. We demonstrated that the co-administration of zebularine, an inhibitor of CR deaminase, with 5-Aza-CdR increases its activity. Zebularine is also an inhibitor of DNA methylation, which may contribute to the enhancement of the antileukemic action of this combination.     In summary, our preclinical data indicate that the antileukemic activity of 5-Aza-CdR can be enhanced by: 1- increasing his dosage, 2- combining it with HDACi, and 3- preventing its inactivation by CR deaminase. The translation of those preclinical observations into clinical protocols may be effective in patients with advanced leukemia.

Keyphrases: Cancer, 5-Aza-2'-désoxycytidine, Zebularine, SAHA, LAQ824, Cytidine désaminase, Leukemia, Cancer, 5-Aza-2'-deoxycytidine, Zebularine, Phenylbutyrate, SAHA, LAQ824, Cytidine deaminase
L'attraction et la rétention des infirmières dans des programmes de personnes en perte d'autonomie liée au vieillissement: un défi pour les cadres intermédiaires

The results of this research done with middle managers who are the immediate superior to nurses working in programs for persons with loss of autonomy related to aging (PALV), also known as home care, show that it is difficult to attrack new nurses to these programs because of a lack of popularity in the field of geriatrics. In order to attrack candidates to these programs, the managers responsible for the organization of work could promote the challenge of managing health situations which are often complex, the flexible work hours, the autonomy that the nurses have in scheduling their route, the fewer weekends of work as compared to hospitals and the lack of obligatory overtime. According to the managers there are no more departures from these programs than for other programs. To further support this retention, managers must put into place a well developed orientation and structure for nurses, mechanisms must be instituted for formal performance evaluations,close attention must be paid to the equitable distribution of tasks, and efforts must be made to guide nurses to function as case mangers and to benefit from assigning tasks to nursing assistants. To sensitize them to the importance of the notion of the client taking charge of their health, pertinent continuing education activities must be developed and offered to nurses based on an analysis of their particular needs, and finally, specific workloads must be offered to nurses 55 years of age and older in order to keep them at work.

Keyphrases: homecare, geriatric, managers, organization of work
Effets de l'entraînement en résistance sur le regain de poids et l'inflammation chez des femmes post-ménopausées en surpoids ou obèses

Objectives: To evaluate if a 1-year resistance training program improved weight loss maintenance and the inflammatory profile in overweight and obese postmenopausal women. The second objective of this study was to determine if the variation in visceral adipose tissue was associated with the changes in inflammatory markers concentrations. Methods: Seventy overweight and obese postmenopausal women were randomized to a control group or a resistance training group. Body composition (dual energy X-ray absorptiometry and computed tomography) and inflammatory markers (C-reactive protein, orosomucoid, haptoglobin) were measured before and after the 1-year weight loss maintenance intervention. Results: Following the weight loss maintenance intervention, we observed a significant body weight and fat mass regain in the control group and the resistance training group (p < 0.05). Significant reductions in orosomucoid and increases in haptoglobin concentrations were noted in both groups (p < 0.05). The variation in visceral adipose tissue was only associated with the changes in C-reactive protein concentrations (r = 0,373, p < 0.05).   Conclusion: Our results suggest that resistance training do not improve weight loss maintenance and the inflammatory profile in overweight and obese postmenopausal women. Moreover, our results indicate that the variation in visceral adipose tissue may not be a key factor implicated in the changes in inflammatory markers concentrations.

Keyphrases: Resistance training, Weight loss maintenance, Obesity, Postmenopausal women
Étude du rôle de l’auto-antigène nucléaire centromérique B (CENP-B) et des auto-anticorps anti-CENP-B dans l’activation des cellules musculaires lisses vasculaires : implication potentielle dans la pathophysiologie de la sclérose systémique

CENP-B is a highly conserved, centromere associated protein and is a major autoantigen in systemic sclerosis (SSc). Anti-CENP-B autoantibodies are associated with prominent vascular manifestations such as pulmonary arterial hypertension (PAH) in the limited cutaneous subset of SSc. PAH occurs as a consequence of progressive obliteration of small arteries due to vascular smooth muscle cell dysfunction, migration and proliferation. However, the factors driving this obliteration are unknown. Earlier in vitro studies have demonstrated that some autoantigens have an additional role when they are released in the extracellular environment during the course of injurious insults resulting in cell death. Indeed, it was previously suggested that extracellular autoantigens participate in normal wound repair processes by acting like cytokines and/or chemokines and subsequently displaying pathogenic activities that contribute to the development of autoimmune diseases. Our present findings suggest that the nuclear autoantigen CENP-B can be added to this set of bifunctional molecules. The present study clearly indicates that exogenous CENP-B bound specifically to the surface of human pulmonary artery SMCs. Binding of CENP-B to SMC stimulated their migration during in vitro wound healing assays, as well as their secretion of interleukins 6 and 8. The mechanism by which CENP-B mediated these effects involved the focal adhesion kinase, Src, ERK1/2, and p38 MAPK pathways. Moreover, CENP-B released from apoptotic endothelial cells was found to bind to SMC, thus indicating a plausible in vivo source of extracellular CENP-B. Here, we also report several lines of evidence indicating that CENP-B, which has no obvious primary or secondary structural homology to chemokines, induced SMC activation by interacting with CCR3. Moreover, the present study clearly demonstrates the involvement of EGFR in CENP-B signaling leading to IL-8 secretion. Finally, anti-CENP-B autoantibodies were found to abolish this signaling pathway, thus preventing CENP-B from transactivating EGFR and exerting its cytokine-like activities toward vascular SMCs. The present study sheds new light on the possible role of extracellular CENP-B and its potent biological effects on human pulmonary artery SMCs. The identification of CENP-B as a CCR3 ligand opens up new perspectives for the study of the pathogenic role of anti-CENP-B autoantibodies.

Keyphrases: CENP-B, anti-CENP-B, CCR3, Transactivation EGFR, Systemis sclerosis, Pulmonary artery hypertension, vascular smooth muscle cells, CENP-B, bifontional autoantigen, anti-CENP-B, CCR3, EGFR transactivation
Mécanismes traductionnels impliqués dans la potentialisation à long-terme de la transmission synaptique des cellules pyramidales de l’hippocampe chez le rongeur

Learning and memory are complex processes that are not yet fully understood at the cellular and molecular levels. It is however widely accepted that persistent modifications of synaptic connections, like long-term potentiation (LTP), could be responsible for the encoding of new memories. These changes are frequently studied in the hippocampus, a temporal lobe structure that as been shown to be necessary for explicit memory in mammals. Long-term potentiation is classically defined as a persistent and stable modification of synaptic connections that have been repeatedly stimulated. Moreover, there are two different phases of LTP: an early-LTP, that only requires the modification of pre-existing proteins, and a late-LTP, that requires the synthesis of new proteins. Numerous studies have evaluated the role of new protein synthesis for the persistence of LTP, however, the mechanisms coupling synaptic activity and the translational machinery, as well as the identity of the necessary proteins are not yet fully understood.  From this perspective, this Ph.D. thesis has evaluated the interactions between synaptic activity and the regulation of translation. As it is widely accepted that the regulation of translation is primarily at the initiation level, we therefore investigated the modulation of two major pathways for the regulation of translation during LTP: the GCN2/eIF2α pathway and the mTOR pathway.  First, our studies have shown that the regulation of the GCN2/eIF2α pathway and of the ternary complex formation are necessary for the long-term maintenance of synaptic plasticity and memory. Indeed, synaptic activity regulates GCN2 and eIF2α phosphorylation, which modulates the transcription factor ATF4 levels. ATF4 in turn regulates CREB-dependent transcription, and therefore controls the levels of genetic expression and the synthesis of new proteins necessary for the long-term stabilization of synaptic modifications.  Moreover, the regulation of the mTOR pathway and of the specific translation of 5’TOP mRNAs likely also play an important role for long-term synaptic plasticity. Modulation of this cascade by synaptic activity specifically increases the translational capacity of activated synapses, allowing them to translate and incorporate the necessary proteins for the lasting reinforcement of synapses.  These studies will undoubtedly help to understand the regulation of translational mechanisms by synaptic activity and their significance for the maintenance of long-term potentiation and long-term memory.

Keyphrases: GCN2, eIF2α, mTOR, Hippocampus, Synaptic plasticity, Long-term potentiation (LTP), Translation, GCN2, eIF2α, mTOR
Les mécanismes endogènes de modulation de la douleur et leur dysfonction dans le syndrome de l'intestin irritable

Pain is a subjective experience comprising multiple dimensions and is accompanied by physiological responses. These responses are regulated by neural processes that play a crucial role in cerebral and spinal modulation of pain. However, the mechanisms of this regulation are still not clear and a better understanding of these processes is essential in order to treat pain effectively. The four studies of this thesis were intended to define the central mechanisms of endogenous pain modulation by counterirritation (application of two competing noxious stimuli) and to investigate the dysfunction of these mechanisms in female patients with irritable bowel syndrome (IBS).  First, an experimental model was developed in which functional magnetic resonance imaging was used to measure brain activity concurrently to the recording of the nociceptive flexion reflex (RIII: an index of spinal nociceptive processes) and skin conductance responses (SCR: an index of sympathetic activation). The first study indicates that individual differences in shock-evoked brain activity in the orbitofrontal (OFC) and cingulate cortices are associated with individual differences in pain sensitivity, motor reactivity (RIII), and autonomic reactivity (SCR) in healthy volunteers. In the second study, it is shown that counterirritation analgesia produced in healthy volunteers is accompanied by the inhibition of the amygdala by the OFC, and the inhibition of the RIII reflex by the periacqueductal gray matter (PAG) and the primary somatosensory cortex (SI). In the third and fourth studies, pain and RIII reflex were not significantly modulated by counterirritation in patients with IBS in comparison to healthy controls. Furthermore, the severity of psychological symptoms was associated with pain modulation deficits and diffuse hypersensitivity in IBS patients. Together, the results of these studies clarify the functions of pain-related activity in specific brain structures and the mechanisms underlying counterirritation analgesia. Moreover, it is concluded that patients with IBS show a dysfunction of cerebral and spinal processes involved in both the perception and modulation of pain.

Keyphrases: modulation, IRMf, brain, spinal cord, pain, Irritable bowel syndrome, modulation, counterirritation, nociceptive reflex, skin conductance response, fMRI, electrical stimulation