The purpose of this study was to examine the radiographic and histologic response. to corundum blasted implant surfaces of varying roughness in a canine total hip arthroplasty model. Three types of tapered femoral implants were made from titanium alloy and were identical in every respect except surface finish. The entire surface of the femoral implant possessed either a 2.9, 4.2 or 6.7 micrometer average surface roughness (Ra) from blasting with 60, 24, or 16 grit corundum particles, respectively. Staged bilateral total hip arthroplasties were performed such that each dog received a 60 grit on one side and a 24 grit or 16 grit implant on the contralateral side. Twenty-two stems in 11 dogs were evaluated at 6 months. The appearance of the bone implant interface was qualitatively characterized. Bone apposition and average bone-implant contact length were determined. Twenty-one of the stems demonstrated osseointegration while one stem developed a stable fibrous interface. All three types of corundum blasted implants demonstrated consistently high amounts of bone apposition, averaging 30.5%. Abundant new peri-implant bone consistently formed, particularly within the intramedullary canal where trabeculae spanned implant-cortical gaps up to 5 mm and established osseointegration ration. There was no statistical difference amongst bone apposition with the 60, 24, and 16 grit stems which averaged 31.7%, 32.0% and 27.9% respectively. However, the pattern of new bone formation was different in that the average length of each region of bone apposition for the 60 and 24 grit surfaces was 50% greater than that for the coarser 16 grit surface (p < 0.02). Through detailed qualitative and quantitative radiographic and histologic elucidation of the osseous response to corundum blasted hip implant surfaces, this study provided new understanding of their potential for biologic fixation. Corundum blasted surfaces represent an important and valuable technology for the design of non

Histone acetylation plays an important role in regulating chromatin structure and thus gene expression. Analysis of histone deacetylase (HDAC) activity in S. cerevisiae revealed the presence of two deacetylase complexes, one containing Hda1 as its catalytic subunit, and the other possessing Rpd3. The three previously identified human HDAC proteins, HDAC1-3, were found to be homologs of Rpd3. This observation suggested that mammalian cells might contain an uncharacterized class of biochemically distinct Hda1-like proteins. The goal of my project has been to identify and characterize mammalian HDAC proteins which are similar to Hda1. I first identified the human histone deacetylase HDAC4, which contains a carboxy-terminal region significantly similar to the catalytic domain of yeast Hda1. When tethered to a promoter, HDAC4 functions as a transcription corepressor. Furthermore, HDAC4 interacts with the transcription factors MEF2 and RFXAf\lK and represses transcription of their target genes, supporting the notion that HDAC4 is a transcription corepressor in vivo. Surprisingly, HDAC4 is localized mainly in the cytoplasmic region and shuttles between the nucleus and the cytoplasm. Nucleocytoplasmic shuttling of HDAC4 is controlled by multiple mechanisms. HDAC4 possesses a nuclear localization signal (NLS) and a nuclear export signal (NES) for its dynamic nucleocytoplasmic trafficking. Binding of 14-3-3 proteins exposes the NES of HDAC4, which then results in its nuclear export. From this work, I have identified HDAC4 and shown that it functions as a transcription corepressor whose activity is regulated by nucleocytoplasmic shuttling.

The terminal events leading to periprosthetic osteolysis are multifactorial and attempts to modulate this process after the stage of modulator release have been futile. Cell death at the osteolytic interface of failed total hip arthroplasties (THAs) may occur via one of two modes---Apoptosis (programmed cell death/cellular suicide) vs. Necrosis. Apoptosis (PCD) is an active form of cell death that results in---among other things---orderly fragmentation of DNA and specific protein synthesis. The purpose of this study was to determine the mode of cell death at this interface. TdT-mediated dUTP nick end-labeling (TUNEL) stain and immunodetection of terminin protein were used to identify apoptosis. / Our studies demonstrated that 31% (range 7--56%) of cells of pseudomembrane were positive for TUNEL stain. Moreover, the presence of apoptosis was the same at both the femoral and acetabular sides of the prostheses. In addition, pseudomembrane (PM) specimens stained for the 30 kDa terminin protein, an apoptosis-specific protein. The results demonstrate that apoptosis is occurring at the PM-bone interface of THAs suggesting that apoptosis, related events may be associated with periprosthetic osteolysis.

A prospective, randomized, experimental study was performed to assess the treatment of mandibular continuity defects by distraction osteogenesis, using the rabbit model. This method of treatment was compared to a control group, which had treatment by traditional means, using a fixation plate. Eight animals were randomized into one of the two groups. / The treatment methods were assessed by clinical, radiographic, and histologic examinations. / Clinically, the experimental specimens had greater dimensions of bone formation in the defects than their matched controls. / Radiographically, there was a higher percentage of radiopacity in the defects of the experimental group compared to the controls, although not statistically significant. / Histologically, there was a statistically significant higher percentage of bone fill in the defects of the experimental group compared to the controls. Three of the four experimental specimens (75%) developed bony union at the 'docking site'. / A cost-efficient animal model was developed for the study of bifocal distraction in the treatment of mandibular continuity defects. The critical-sized mandibular defect in the rabbit model was found to be a minimum of 4mm.

In the context of the choice of treatment for end-stage renal disease, three approaches to utility assessment were examined to determine which captures prospective patients' values best. The standard gamble (SG), time tradeoff (TTO) and visual analogue scale (VAS) were compared for their test-retest reliability and convergent validity. The study population consisted of patients who attended nephrology clinics at one of three teaching hospitals in the city of Montreal. Sixty-six patients were interviewed three times by one of two interviewers. They were taught about the treatments using an information package developed expressly for the study and a video produced by a pharmaceutical company for use in this decision context. Utilities for treatment were measured on two occasions about one week apart. / Patients differed widely in the utilities provided (responses ranged from 0 to 100) but mean utilities were similar across the treatments assessed. Because of the wide variation among subjects, the intraclass correlation coefficients for test-retest reliability were high to moderate: 0.87 for SG, 0.73 for TTO and 0.64 for VAS. However, the precision of the methods, as measured by the standard deviation of the measure from one occasion to the next within subjects, was low with SD's of 10 for SG, 14 for TTO and 13 for VAS assessments. The use of correlation coefficients as a measure of reliability and convergence in this context was challenged. / SG and TTO utilities and SG and VAS utilities (when anchoring effects were controlled) were unbiased estimates of one another, but the degree of agreement between each pair was low. The VAS assessments produced higher values than the TTO assessments. Both SG and VAS were susceptible to strong anchoring effects; in other words, the utilities obtained were different when the best and worst outcomes used to anchor the ends of the scale were changed from full health and death to full health and the worst treatment. / Subject characteristics and study factors were investigated for associations with reliability and with convergence and with the absolute level of utility. The standard gamble approach was strongly associated with many of the factors, while the time trade-off and the visual analogue utilities were associated with fewer. / The poor reliability of the methods raises questions about their use in decision aids for individuals. The lack of agreement among the methods indicates that the methods cannot be used interchangeably.

Certain regions adopt an aggressive approach (routine cardiac catheterization and frequent invasive revascularization) to care for acute myocardial infarction (AMI), while other regions adopt a conservative approach (selective use of invasive procedures). Administrative data provide a means to estimate the effects of these variations on patient outcomes, but they are limited by their potential for confounding bias due to unobserved case-mix variation as treatment assignment is not random. This study applied instrumental variables, a methodology that can account for this bias, to estimate the effectiveness of aggressive care in a Canadian patient population. The study used administrative data of hospital admissions and health services for all patients admitted for a first AMI in Quebec in 1988 (n = 8674). Incremental (marginal) mortality up to 4 years after admission was measured using distances to hospitals offering aggressive care as instrumental variables. / Patients living closer to hospitals offering aggressive care were more likely to receive aggressive care than patients living further away (e.g. 26% versus 19%, respectively, received catheterization within 90 days). However, instrumental variable estimation found that aggressive care was not associated with marginal mortality benefits in comparison to conservative care (e.g. adjusted difference at 1 year: 4%; 95% CI: -11% to 20%). / The aggressive approach to post-AMI care is not associated with marginal mortality benefits in Quebec.

There has been an explosion in our understanding of the intimate relationship between inflammation and cancer. One aspect of this relationship is the observed poor oncologic outcomes amongst patients having suffered infectious complications from surgery for their malignancy. Although little is known about the role of neutrophils in the metastatic cascade, they are the prime cellular effectors of the acute inflammatory response and heavily recruited to common metastatic sites such as the liver during states of acute inflammation. Our underlying hypothesis was that the combination of heavy neutrophil recruitment to liver sinusoids in the presence of circulating tumor cells would create a fertile ground for the seeds of metastasis. A physiologically relevant in vivo model of early metastasis coupled with intravital microscopy was used to visualize the trafficking of tumor cells within the liver vasculature in real time. Systemic inflammation induced by lipopolysaccharide significantly enhanced the metastatic potential of cancer cells by increasing their propensity to adhere to the liver sinusoidal endothelium. Disrupting the interactions between inflammation inducible endothelial selectins and tumor cell selectin ligands diminished tumor cell recruitment to the liver and reversed the effects of lipopolysaccharide. Confocal microscopy revealed frequent colocalization of cancer cells with neutrophils and neutrophil depletion in vivo significantly attenuated cancer cell adhesion and gross metastasis. Mac-1/ICAM-1 interactions mediated this effect. Neutrophils acted as a tethering anchor for circulating tumor cells in the liver. A novel neutrophil-mediated mechanism of metastatic recruitment was identified via neutrophil extracellular traps. Together these findings constitute some of the first mechanistic studies to implicate neutrophils in the metastatic process and as an important target to diminish the occurrence of metastasis amongst cancer patients. / Notre compréhension de la relation intime entre la progression cancéreuse et l'inflammation connait une croissance importante. Un aspect de cette relation est la piètre survie des patients atteints du cancer qui subissent une complication infectieuse suite a une chirurgie visant l'élimination du cancer en question. Bien que peu soit connu sur le role des neutrophiles dans la cascade métastasique, ces cellules sont les princpaux effecteurs de la réponse inflammatoire aiguë. Notre hypothèse sous-jacente était que la combinaison entre un recrutement important de neutrophiles aux sinusoides hépatiques en la présence de cellules tumorales circulantes offre un sol fertile à l'implantation de métastases. Un model in vivo physiologique pertinent des métastases hépatiques précoces couplé avec la microscopie intravitale a été utilisé pour visualizer le trafic des cellules tumorales dans les sinusoides hépatiques en temps réel. L'inflammation systémique induit par l'administration de lipopolysaccharide augmenta significativement le potentiel métastasique des cellules cancéreuses en augmentant l'adhésion à l'endothélium sinusoidal hépatique. L'interruption des interactions entre les sélectines endothéliales induites par l'inflammation et les ligands de sélectines présents sur les cellules tumorales a eu pour effet de réduire le recrutement des cellules tumorales au foie et renversa les effets de la lipopolysaccharide. La microscopie confocale révéla une colocalisation fréquente de cellules tumorales avec des neutrophiles. La cytoréduction des neutrophiles a eu pour conséquences de réduire l'adhérence des cellules tumorales ainsi que de réduire les métastases macroscopiques. Les interactions entre Mac-1 et ICAM-1 étaient responsables pour cet effet. De plus, les neutrophiles agissent comme une ancre pour les cellules tumorales circulantes. Finalement, un nouveau méchanisme métastasique fut indentifié où les pièges extracellulaires neutrophiliques sont capables decapter les celllules tumorales circulantes. En somme, ces trouvailles constituent parmis les premières à démontrer que les neutrophiles ont un role important lors du processus métastasique et qu'elles forment une cible importante pour limiter l'apparition des métastases chez les patients atteints du cancer.

It is increasingly recognized that because humanitarian healthcare workers are trusted to provide support and assistance to vulnerable groups and populations, they have a fiduciary responsibility rendering it important for them to be explicit and thoughtful about how and why they make ethical choices. This thesis explores the ethics of humanitarian healthcare aid and examines how health care professionals can best engage with these issues, from the realm of ideal ethical theory, to the realm of applied ethical analysis tools. It begins with a brief introduction outlining important elements in the history, ideology and ethics of humanitarian healthcare aid. The second chapter provides an overview of how ethical theory, notably: deontology, consequentialism and virtue ethics, underlies and informs humanitarian healthcare aid responses. I argue that familiarity with ethical theory improves moral clarity and enhances ethical deliberation. The realm of ideal ethical theory is at times abstract and so ethical analysis tools have been developed to assist clinicians in day-to-day ethical deliberation. Many argue that ethical analysis tools facilitate more comprehensive and systematic deliberation of ethical issues arising in a variety of healthcare contexts. However, the strengths and limitations of these tools have received little scrutiny or empirical investigation. Chapter three, provides an analysis of the strengths and limitations of analysis tools, and proposes questions for further research and development in four key areas: for what purpose is the tool developed, who is it designed for, when should tools be used, and what is the structure of the tool? I argue that responding to these questions is a requisite step if ethics analysis tools are to continue to be developed and published. Chapter four unites themes from Chapters two and three by presenting a research study investigating the usefulness of a humanitarian healthcare ethical analysis tool (HHEAT) designed to assist humanitarians in the field. Participants in this study were unanimous that the HHEAT helped ensure comprehensive and more organized ethical deliberation, and expressed a preference for a shorter, more concise tool. This study is notable in presenting one of the few attempts to empirically investigate the usefulness of an ethics analysis tool. Based on participant feedback, the HHEAT was shortened and an accompanying handbook was developed. In Chapter five, I conclude that ethical theory and applied analysis tools present mutually reinforcing approaches to ethical deliberation. When used in tandem, each has the potential to enhance ethical deliberation, analysis and justification, which are essential to humanitarian healthcare practice. / On reconnaît de plus en plus que les travailleurs humanitaires, auxquels on fait confiance pour fournir soutien et assistance aux populations et groupes vulnérables, ont une responsabilité fiduciaire et qu'il est important pour eux d'être explicites et réfléchis sur le comment et le pourquoi lorsqu'ils font des choix éthiques. Cette thèse explore l'éthique de l'aide humanitaire et examine quelle est la meilleure façon de traiter de ces questions à partir du domaine de la théorie éthique idéale et du domaine de l'éthique appliquée et des outils d'analyse éthique. La thèse débute avec une brève introduction exposant des éléments importants dans l'histoire, l'idéologie et l'éthique de l'aide humanitaire. Le deuxième chapitre donne un aperçu sur la façon dont la théorie éthique, notamment, la déontologie, le conséquentialisme et l'éthique de la vertu, sous-tend et façonne les réponses humanitaires. Je soutiens qu'une connaissance de la théorie éthique améliore la clarté morale et la délibération éthique. Toutefois, le domaine de la théorie éthique idéale est parfois abstrait et des outils d'analyse éthique ont été développés pour aider les cliniciens dans la délibération éthique quotidienne. Beaucoup soutiennent que les outils d'analyse éthique facilitent une délibération plus complète et plus systématique des problèmes éthiques qui se posent dans une variété de contextes de soins. Cependant, la force et les limites de ces outils n'ont pas été examinées ou validées empiriquement. Dans le chapitre 3, une analyse des points forts et des limites des outils de l'analyse est présentée et des questions pour de futurs projets de recherche sont proposées dans quatre domaines clés: Dans quel but l'outil est-il développé? A qui est-il destiné? Quand ces outils devraient-ils être utilisés? Et quelle est la structure de l'outil? Je soutiens que la réponse à ces questions est une étape indispensable si l'on veut continuer à développer et à publier des outils d'analyse éthique. Le chapitre 4 fait le lien entre les thèmes des chapitres 2 et 3 en présentant le développement et le raffinement d'un outil d'analyse éthique humanitaire (HHEAT) conçu pour aider les travailleurs humanitaires sur le terrain. De façon unanime, les participants à cette étude ont trouvé que le HHEAT a été utile pour assurer une délibération éthique complète et mieux organisée. Ils ont exprimés une préférence pour un outil plus court, plus concis. Cette étude est remarquable car elle représente une des rares tentatives d'investigation sur l'utilité d'un outil d'analyse éthique. En réponse aux commentaires des participants, le HHEAT a été abrégé et un manuel d'accompagnement développé. Dans le chapitre 5, je conclus que l'éthique théorique et les outils d'éthique appliquée présentent des approches qui se renforcent mutuellement dans la délibération éthique. Utilisées en tandem, ces approches ont le potentiel d'améliorer la délibération éthique, l'analyse et la justification qui sont essentiels à la pratique des soins humanitaires.

Traditionally chemotherapy, used for the treatment of breast cancer, relied on combinations containing 5-Flurouracil (5-FU). Recently, to improve the therapeutic index of 5-FU and its oral availability, a new prodrug termed capecitabine (Xeloda ®) was developed. Capecitabine requires enzymatic activation by hepatic carboxylesterase (CES), to generate 5'-DFCR, then 5'-DFUR, the latter in turn is metabolized by thymidine phosphorylase (TP) into 5-FU. The good tolerance of capecitabine has inspired the search for agents with which it can synergize. Many capecitabine-based two-drug combinations have been proposed with different agents, such taxanes and kinase inhibitors with various degrees of success. We hypothesized that approaches that exploit enzymes involved in the activation of capecitabine should lead to strong synergistic modalities. Here, we exploited two such enzymes involved in the metabolism of capecitabine, TP and CES, to design single molecules, termed "combi-molecules" capable of mimicking the combination of capecitabine with an EGFR tyrosine inhibitor. Our rationale design was further strengthened by the initial observation that EGFR inhibition leads to an increase in TP levels. This thesis first defines the pharmacological profile of the EGFR inhibitor + 5'-DFUR combination, which showed a linear correlation between inhibition of the tyrosine kinase of EGFR and enhancement of TP expression (y = 0.02922*x + 0.4642, R2=0.88, P value=0.005). Thus, we designed and synthesized two classes of combi-molecules: one based on the carbamate function of capecitabine that requires CES for activation (5'-DFCR-based combi-molecules) and another containing a linker at the N1 of 5'-DFUR that can be spontaneously hydrolyzed. Our first prototype, ZRX1 (a 5'-DFCR-based combi-molecule) was ineffective when intact. However, when CES was present, ZRX1 induced an increase in EGFR phosphotyrosine inhibition, TP expression, DNA damage and apoptosis. ZRX1 was, at least, 3-fold more potent than capecitabine and 5'-DFUR and recapitulated the effects of the combination. Unfortunately, ZRX1 was deprived of EGFR inhibitory potency (IC50= 4 µM) on its own and required carboxylesterase (CES) activation to elicit optimal effects. Given the fact that intact ZRX1 would not exert strong EGFR inhibitor, we undertook a structure optimization study of our molecules to enhance their EGFR inhibitory potency. The results showed that replacing the ethoxyethyl linker of ZRX1 by amine-containing chains led to combi-molecules with nanomolar range EGFR inhibition IC50 values even when intact. Whether they had their EGFR inhibitory arm grafted on N3 of the sugar, resulting as in the 5'-DFCR-based combi-molecules (CT3-51, and CT3-138) or on the N1, as in the 5'-DFUR-based combi-molecules CT3-55, CT3-127, CT3-1343 and MAT54. These optimized combi-molecules generated activity profiles that mimicked the combination of EGFR inhibitor + capecitabine or metabolite 5'-DFUR. However, in contrast to the 5'-DFCR-based class, the 5'-DFUR-based class did not require the presence of CES to generate its dual EGFR inhibitory and anti-metabolite mechanism of action. Having defined the structural requirement to obtain a potent combi-molecule, we selected one of such molecule to focus on the dissection of the mechanism of action of our novel approach. / Traditionnellement, la chimiothérapie utilisée pour le traitement du cancer du sein comptait sur des combinaisons qui contiennent 5-Flurouracile (5-FU). Récemment, pour améliorer l'index thérapeutique de 5-FU et sa disponibilité par voie orale, un nouveau promédicament nommé capécitabine (Xeloda ®) a été développé. Capécitabine nécessite l'activation enzymatique par l'enzyme hépatique carboxylestérase (CES), pour générer 5'-DFCR, puis 5'-DFUR, ce dernier à son tour est métabolisé par thymidine phosphorylase (TP) en 5-FU. La bonne tolérance de capécitabine a inspiré la recherche d'agents avec lesquels ce médicament peut avoir une synergie. De nombreuses combinaisons de deux médicaments à base de capecitabine ont été proposées avec différents agents, tels que les taxanes et les inhibiteurs de kinases, avec divers degrés de succès. Nous avons avancé l'hypothèse que exploiter des enzymes impliquées dans l'activation de capécitabine devraient conduire à des fortes modalités synergiques. Ici, nous avons exploité deux de ces enzymes impliquées dans le métabolisme de capécitabine, CES et TP, afin de concevoir des molécules uniques, appelés « combi-molécules » capables de mimer la combinaison de capécitabine + un inhibiteur du récepteur EGFR. Notre logique de conception a été renforcée par l'observation initiale que l'inhibition de l'EGFR conduit à une augmentation des niveaux TP. Cette thèse définit d'abord le profil pharmacologique de la combinaison d'un inhibiteur de EGFR + 5'-DFUR, qui a démontré une corrélation linéaire entre l'inhibition de la tyrosine kinase de l'EGFR et l'augmentation dans l'expression de TP (y = 0,02922 * x + 0,4642, R2 = 0,88, P = 0,005). Ainsi, nous avons conçu et synthétisé deux classes de combi-molécules: l'une basée sur la fonction carbamate de capécitabine, nécessitant CES pour être activée (les combi-molécules à base de 5'-DFCR ) et une autre contenant une liaison au niveau du N1 du 5'- DFUR qui peut être hydrolysé spontanément. Notre premier prototype, ZRX1 (une combi-molécule à base de 5'-DFCR) était inefficace sous sa forme intégrale. Cependant, quand CES était présente, ZRX1 a induit une augmentation de l'inhibition d'EGFR, d'expression TP, des lésions à l'ADN et de l'apoptose. ZRX1 était, au moins 3 fois plus puissant que capécitabine et 5'-DFUR et a récapitulé les effets de la combinaison. Malheureusement, ZRX1 manquait de puissance inhibitrice d'EGFR (IC50 = 4 µM) et ne pouvait être activé que dans présence de CES. Vu que ZRX1 n'exerce pas une forte inhibition d'EGFR, nous avons entrepris une étude d'optimisation de la structure de nos molécules, pour améliorer leur pouvoir inhibiteur d'EGFR. Les résultats ont montré que le remplacement de la fonction éthoxyéthyl de ZRX1 par des chaînes contenant des amines a conduis à des combi-molécules avec des valeurs de IC50 d'inhibition de l'EGFR en nanomolaire, même sous leur forme intégrales. Ceci est valable pour les combi-molécules à base de 5'- DFCR qui avaient le bras inhibiteur d'EGFR greffé sur N3 du sucre comme CT3-51, et CT3 – 138 et les combi-molécules à base de 5'- DFUR (CT3 -55 CT3 - 127, CT3-1343 et MAT54) substituées en N1. Ces combi-molécules optimisées ont généré des profils d'activité qui imitent la combinaison d'un inhibiteur d'EGFR + capécitabine ou son métabolite 5'- DFUR. Cependant, contrairement à la classe à base 5'-DFCR, la classe à base 5'-DFUR n'exige pas la présence de CES pour générer son double mécanisme d'action d'inhibiteur d'EGFR et d'anti-métabolite. Après avoir défini l'exigence structurelle pour obtenir une combi-molécule efficace, nous avons choisi une de ces molécules afin de se concentrer sur la dissection du mécanisme d'action de notre nouvelle approche.

In Plastic Surgery, learning objectives have been outlined by the Royal College of Physicians and Surgeons of Canada, however, a defined curriculum to meet these objectives is absent. Several factors are reducing the practicality of the current time-based model and as a result, a competency-based training model has been proposed to replace the traditional model. Implementation of a competency-based curriculum requires several steps including the identification of both specialty specific procedures and procedural steps. The present project aims to develop a methodology for identifying procedural steps for individual Plastic Surgery procedures. Previous studies have highlighted the lack of resident exposure to several areas of Plastic Surgery, particularly aesthetic surgery. Avenues for increasing resident exposure and training opportunities must be explored. An additional aim of this project is to achieve this through the development of a pilot simulator mannequin for aesthetic surgery training. The identification of Plastic Surgery procedural steps together with simulator training is a novel step forward towards implementation of competency-based education in Plastic Surgery training. / En chirurgie plastique, le Collège royal des médecins et chirurgiens du Canada propose des objectifs d'études bien définis, cependant il n'y a pas de curriculum défini afin d'atteindre ces objectifs. Plusieurs facteurs réduisent l'aspect pratique du modèle en fonction du temps existant, et comme résultat, le modèle d'enseignement basé sur la compétence fut proposé pour remplacer le modèle traditionnel. La réalisation d'un curriculum basé sur la compétence demande autant l'identification des procédures spécifique de cette spécialité que des étapes procédurales. Ce projet tend à développer une méthodologie pour l'identification des étapes procédurales pour chacune des procédures de la chirurgie plastique. Les études précédentes ont démontrées que les résidents manquent d'exposition aux connaissances de plusieurs domaines de la chirurgie plastique, particulièrement vrai pour la chirurgie esthétique. Il est donc important, pour les résidents, d'explorer tous les avenues pour augmenter cette exposition et leurs opportunités de formation. La cible additionnelle de ce projet est d'atteindre ces objectifs par le développement d'un mannequin-simulateur pilote pour l'entraînement en chirurgie esthétique. L'identification des étapes procédurales en chirurgie plastique, en concert avec l'entraînement par simulateur, engendre une nouvelle étape vers la réalisation d'une éducation basée sur la compétence en chirurgie plastique.