This research delves into idiopathic autism spectrum disorder (ASD), investigating the role of TrkB signaling pathways and BDNF regulation in the cortex. Additionally, it explores offering insights into maternal influences on mouse models. / Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by challenges in social interactions and repetitive behaviors. Prevalence of ASD is estimated to be 1 in 54 globally and is rising recently in many countries including Canada. ASD affects individuals differently, making diagnosis challenging. At present, no molecular diagnosis of ASD is available. Further, available medications only manage some symptoms of the disease and have adverse side effects in children. Therefore, there is a need for accurate molecular diagnostic tools to aid in molecular detection and treatment of ASD. To this end, a better understanding of the underlying molecular mechanisms that link ASD etiology to ASD-related behavior is crucial. While genetic factors contribute to syndromic ASD, most cases of ASD are idiopathic with unknown causes, influenced by a combination of epigenetic and environmental factors. TrkB and its downstream signaling pathways, such as Akt and Erk, are hyper-activated in syndromic ASD and hypo-activated in idiopathic cases. Therefore, drugs like rapamycin that inhibit the mTOR pathway downstream of TrkB are beneficial for syndromic ASD but not idiopathic cases. Additionally, insulin-like growth factor 1 (IGF-1), which mitigates ASD-related synaptic disruptions via Akt and Erk signaling, shows unchanged mRNA and protein levels along with its receptor in the idiopathic ASD fusiform gyrus. In ASD with either genetic or epigenetic/environmental causes, disruptions in synaptic connectivity are observed. Synaptic function is regulated by signaling pathways involving brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase B (TrkB), as well as their downstream signaling cascades such as MAPK and Akt. The existing literature suggests that there is an association between BDNF and TrkB signaling pathways and ASD. However, a serious gap in knowledge about the precise molecular role of TrkB in ASD pathology is that our current understanding is correlational in nature and based on observational studies that lack causal experiments. This underscores the importance of further research to understand the causative role of TrkB and its related molecular events in idiopathic ASD. The present work aims to provide a deeper understanding about the causative role of molecular mechanisms underlying TrkB signaling in ASD. ASD mouse models exhibit behaviors and molecular features resembling those observed in human ASD. Therefore, these mouse models are helpful tools for studying ASD. However, understudied physiological confounding factors, such as maternal age and parity, can introduce biases and add to data variability, thus negatively impacting the reproducibility and translational value of ASD mouse models. To achieve a reliable mouse model of ASD, we conducted our first study that examines the impact of maternal age and parity on pregnancy complications, neurodevelopment, and social behavior in mice. Results demonstrate that older maternal age and prior motherhood interact to ensure a normal, steady developmental rate and provide protective effects against anxiety, social impairment, and olfactory deficits. Given the current lack of clarity regarding the causative impact of TrkB on ASD pathology, our subsequent investigation sought to establish a causal relationship between TrkB signaling and ASD. We used the TrkB agonist, LM22A-4 treatment in a validated ASD mouse model. Our results demonstrate that treatment with LM22A-4 effectively rescues the core symptoms associated with ASD (social impairment and repetitive behavior). These findings indicate that impaired TrkB signaling is responsible for ASD-like behavior of valproic acid (VPA)-exposed mice. However, unlike TrkB-related molecular events occurring in the fusiform gyrus of idiopathic ASD, TrkB isoform protein levels, BDNF species, Akt, and Erk total protein levels and activation remained unchanged in VPA-exposed cortices compared to healthy control mice. Since our VPA mouse model does not replicate human idiopathic ASD, our study cannot draw a conclusion on how disruptions in these signaling pathways may contribute to the development and manifestation of ASD symptoms. Cortex is responsible for various aspects of social behavior that are impaired in ASD. However, regulatory mechanisms that are involved in ASD upstream of cortical TrkB and BDNF are not well known. BDNF expression is highly cell-and tissue-specific and is regulated by different sets of transcription factors in specific tissues. While NURR1, the BDNF regulator in midbrain neurons, is associated with ASD pathology, its specific role in regulation of cortical BDNF is not yet well-established. Our third study aimed to understand the role of NURR1 in regulating BDNF specifically in the cortex. We showed that in resting and depolarized neurons, when NURR1 is knocked down, BDNF mRNA levels remained unchanged, suggesting that NURR1 does not regulate BDNF in cortical neurons and highlighting the tissue-specificity of BDNF regulation. In summary, we address the understudied effects of maternal factors on mouse models, which enhances the reliability of ASD research. Further, our studies significantly enhance the understanding of ASD by elucidating the role of TrkB and its downstream signaling pathways in the behavioral aspects of the disorder. We also contribute to the knowledge of BDNF regulation in the cortex, a brain tissue with crucial roles in various aspects of social behavior. In a forward-looking approach, the results of our studies provide valuable insights into mouse modeling of idiopathic ASD and the potential role of TrkB in ASD behavioral symptoms. / Thesis / Candidate in Philosophy / Autism spectrum disorder (ASD) is a condition that is accompanied by challenges in social interaction and repetitive behaviors. ASD is a complicated condition because we do not fully understand all the details of how it works in the body. Studying ASD is important as it is the most challenging condition in children and it is becoming more common, especially in the last two decades. While scientists are developing molecular tools to improve ASD diagnosis and understand its biology, these tools are not widely used in clinics for ASD diagnosis yet. Also, the approved medications available can only help with managing some of the behavioral symptoms like self-harming behavior. Despite the pressing need to find a solution, our recent advancements have not yet brought us closer to a cure for ASD, mainly because of the complexity of the disorder. Therefore, identifying the specific ASD-related mechanisms at the molecular level that contribute to ASD-related behaviors is crucial for gaining a deeper understanding of the disease. In ASD, there are problems with how brain cells communicate with each other. This communication is controlled by certain molecules in the brain, such as brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase B (TrkB), along with other molecules. There is evidence suggesting a link between these molecules and ASD, but we have not fully understood their precise roles because most of the current knowledge is based on observations and correlations, rather than on establishing cause-and-effect relationships. To bridge this gap, our research focused on understanding TrkB's role in ASD. We required reliable mouse models. Since we aimed to induce ASD-like behaviors in mice using an ASD-causing chemical, it was crucial to ensure they were healthy beforehand. We needed to confirm that any social deficits or repetitive behaviors were not due to other factors, such as adverse infancy experiences or impaired interactions between mother and infant. We discovered that sexually mature dams aged between 3 to 6 months, with a history of previous pregnancies and motherhood, give birth to healthier litters. These litters can serve as a more dependable source for our animal behavioral studies. Many cases of ASD in humans are caused by non-genetic factors such as environmental influences like pesticides, air pollution, and the use of certain drugs during pregnancy. In cases of human ASD triggered by non-genetic factors, there is an increase in proBDNF, the precursor of BDNF. However, this proBDNF does not efficiently convert to BDNF. With insufficient BDNF and TrkB receptors, molecules like Akt (protein kinase B, also PKB) and Erk (Extracellular Signal-Regulated Kinase), which are crucial for neuron communication, are also less active downstream. This imbalance disrupts neuron connections, leading to ASD behaviors. In our research, the ASD-causing chemical which we used is valproic acid. It is originally an anti-seizure medication. When pregnant women took valproic acid, the chance of their child having ASD increased. Scientists used this information to inject pregnant mice with valproic acid, and as a result, all the offspring showed ASD-like behaviors. We anticipated that by isolating the brains of these offspring and measuring protein levels of BDNF, TrkB, Akt, and Erk, we would observe a similar pattern to that seen in humans with non-genetic ASD cases. We focused on studying the cortex, a region of the brain responsible for regulating social behaviors in both mice and humans. Since ASD is associated with challenges in social behaviors, we isolated the cortex from mouse brains to analyze protein levels. A chemical known as LM22A-4 with a structure resembling BDNF can bind to TrkB and activate it. We expected that the offspring of pregnant dams injected with valproic acid, which led to reduced TrkB axis activation in their brains, would show improvement in ASD behavior. This anticipation stems from the understanding that LM22A-4 activates the TrkB axis, thus compensating for its reduction, which is thought to be causing ASD-like behaviors. The offspring of mothers injected with valproic acid exhibited ASD-like behaviors, unlike the control mice. Control mice were offspring of pregnant dams injected with a solution containing only the substances used to dissolve valproic acid, typically water and salt (saline). Mice prenatally exposed to valproic acid (VPA) exhibited ASD-like behaviors, but treatment with LM22A-4 helped alleviate these behaviors, promoting more typical behavior patterns. LM22A-4, by activating TrkB receptors, helped to protect the brain from harm caused by exposure to valproic acid before birth. This could mean that valproic acid-induced changes in TrkB-related molecular mechanisms are involved in social behavior difficulties and increased repetitive behaviors seen in autism. Nevertheless, the levels of TrkB, BDNF, proBDNF, Akt, and Erk in the cortex of offspring from mothers injected with valproic acid were like those in the offspring from mothers injected with the saline solution. Therefore, the BDNF and TrkB signaling pathways remained unchanged in the cortex of our valproic acid model in this study, and they differ from those observed in human idiopathic ASD. We also speculated that a protein, called NURR1 acting upstream of BDNF and TrkB might be involved in the process. NURR1 acts as a regulatory protein that binds to the BDNF, increasing the production of copies from the BDNF. We also used a small RNA that targets a specific region in the Nurr1 and inhibits its protein production We anticipated a reduction in Nurr1 levels. As NURR1 acts as an upregulator of BDNF, lower levels of Nurr1 would result in decreased BDNF production. Activating NURR1 resulted in increased BDNF mRNA levels. However, when NURR1 was reduced, BDNF mRNA levels remained unaffected. This led us to conclude that if NURR1 levels decrease, other proteins may step in to maintain BDNF mRNA levels. Therefore, in the cortex, unlike in some other brain regions, the presence of NURR1 is not essential for regulating Bdnf. In summary, before inducing ASD-like behavior in mice using valproic acid, it is crucial to ensure the health of the mice. We used sexually mature mothers with prior pregnancy experience to provide a healthy baseline. We showed valproic acid induced ASD-like behaviors in mice offspring. We also observed that LM22A-4 treatment alleviated ASD-like behaviors of offspring. In our study, we demonstrated that the levels of BDNF, TrkB, Erk, and Akt proteins in the cortex of mice exposed to valproic acid were not affected. For this reason, our mouse model does not resemble human non-genetic ASD. Finally, NURR1's role in BDNF regulation varies by brain region. Lowering NURR1 did not affect BDNF mRNA levels, suggesting compensatory mechanisms. Our findings suggest new directions for further research to better understand the roles of TrkB and BDNF in non-genetic ASD. Overall, this study provides valuable knowledge that can contribute to advancing our understanding of idiopathic ASD-related molecular mechanisms.

[pt] Tradicionalmente, muitos trabalhos têm estudado os efeitos das intervenções cambiais esterilizadas nas taxas de câmbio, tanto empiricamente quanto teoricamente, encontrando resultados mistos. Mais recentemente, a literatura de finanças internacionais têm procurado explicar os desvios na Paridade Coberta da Taxa de Juros (PCJ), que vem sendo observado entre as moedas das economias desenvolvidas após a Grande Crise Financeira de 2008. Neste trabalho, ligamos as duas literaturas ao estudar o efeito das intervenções cambiais nos desvios na paridade coberta de juros. Nossa amostra consiste nas intervenções realizadas pelo Banco Central do Brasil entre os anos de 2009 e 2020. Este período contempla o programa de intervenções pré-anunciadas de 2013, implementado no contexto do Taper Tantrum, e que já mostrou ter afetado significantemente as taxas de câmbio (Chamon, Garcia e Souza (2017) ). Para avaliar os efeitos, construímos uma série contrafactual utilizando a metodologia ArCo, desenvolvida por Carvalho, Masini e Medeiros (2018), e também estimando funções impulso resposta utilizando Local Projection, desenvolvida por Jordà (2005). Os resultados indicam que a venda de dólares no mercado futuro aumentam os desvios na PCJ, enquanto que compras de dólares tem o efeito oposto. A oferta de dólares via contratos de recompra diminui os desvios no curto prazo. As intervenções no mercado a vista apresentam resultados inconclusivos. / [en] Traditionally, much has been written about the effects of FX (foreign exchange) sterilized interventions on exchange rates, both theoretically and empirically, with mixed results. More recently, the international finance literature has tried to explain the deviations from the well-known Covered Interest Parity (CIP) condition that have, since the 2008 Great Financial Crisis, arisen among advanced economies currencies. Here, we originally merge these two strands of the literature by analyzing the effects of sterilized FX interventions on the CIP (Covered Interest Parity) deviation. Our sample is composed of Brazilian Central Bank FX interventions between 2009 and 2020. This period contains a major program of announced FX interventions in response to the Taper Tantrum, in 2013, which has already been shown to have significantly affected the level of the exchange rate (Chamon, Garcia, and Souza (2017)). To gauge the effects, we build a counterfactual employing the ArCo methodology, developed by Carvalho, Masini, and Medeiros (2018), and also make use of Jordà (2005) Local Projections. The results indicate that selling US dollars in the futures market increases CIP deviations while buying US dollar futures has the opposite effect. Offering US dollar repo credit lines points to a short-lived decrease in the deviation. The number of sterilized sales or purchases of spot currency seems not to be high enough to lead to conclusive results.

Breast cancer poses a serious public health concern. This case-control study describes the relationship of night-shift working on the development of breast cancer in 57 women diagnosed with breast cancer compared to 49 women with other types of cancer in the Vaal Triangle area (selected through non-probability purposive sampling from CANSA). The study revealed that women who work night-shift developed breast cancer 1.24 times more often than women who do not work nightshift (OR=1.24 [95% CI 0.52 to 2.89]). The odds ratio was further increased in women who worked rotating-shift (OR=1.44 [95% CI 0.58 to 3.59]). Night-shift work exposure was not statistically related to the development of breast cancer. It is recommended that the relationship between night-shift exposure and breast cancer risk be further explored through cross-sectional and cohort studies, and other breast cancer pathways. / Health Studies / M.A. (Public Health)

The main objective of the study was to determine the exchange rate volatility regime for carry trade profitability when using the South African Rand as the target currency. The study used the Logistic Smooth Transition Regression (LSTR) model to test the uncovered interest rate parity (UIP). The Sharpe ratio and the risk adjusted forward premium were used as the transition variables. The transition variable is a function of the transition function, which is used to determine the regime for the UIP. The LSTR model is characterised by three regimes, i.e. the lower regime, the middle regime and the upper regime. The LSTR model was tested for the short-term forward rate maturity of less than one year. The results show that the UIP hypothesis holds in the middle regime for the Rand/USD and the Rand/GBP when using the Sharpe ratio as the transition variable. Meanwhile, the UIP hypothesis does not hold for the Rand/Yen when using the Sharpe ratio as the transition variable for the forward rate maturity of one month, and it does hold for other short-term forward rate maturity of less than one year. The results for the risk adjusted forward premium as the transition variable show that the UIP hypothesis does not hold for all three currencies at various short-term forward rate maturities of less than one year. The research provides the following contributions to new knowledge: (1) Uncovered interest parity hypothesis holds in the middle regime for all periods for the Rand/USD and the Rand/GBP when using the Sharpe ratio as the transition variable with a short-term forward rate maturity of less than one year. (2) Currency carry trade profit taking for the Rand/USD and the Rand/GBP can be achieved in the upper regime. (3) The results for the Rand/Yen are mixed, in that the UIP hypothesis does not hold for other crisis periods as a result of negative Sharpe ratios. However, for the calm periods, UIP hypothesis holds in the middle regime for the Rand/Yen for short-term forward rate maturity of more than one month but less than one year when using the Sharpe ratio as the transition variable. The overall contribution of this study is that for the South African Rand as the target currency, the UIP hypothesis holds for the short-term horizon when using the Sharpe ratio as the transition variable and that this mostly depends more on currency than on horizon. Contrary to other researchers who found that the UIP holds in the long-term maturity with higher Sharpe ratios in the upper regime, this study proved that the UIP holds in the short-term maturity horizon. / Business Management / D.B.L.

South Africa is experiencing a financial skills shortage with a severe shortage of accountants and chartered accountants in particular. The aim of this study was to measure accessibility of public higher education in South Africa, in general and specifically relating to accountancy programmes with special emphasis on chartered accountancy programmes in South Africa, by making use of selected accessibility indicators. Although some of these indicators have been used to measure accessibility of higher education in general both locally and internationally, they are not often used to measure accessibility of a programme for a particular profession such as accountancy or chartered accountancy. This study aimed to fill this gap by measuring the selected accessibility indicators and providing subsequent rankings of the four public universities selected for this study. The results can be used by institutions that offer accountancy and chartered accountancy programmes as well as the South African Institute of Chartered Accountants, as the profession’s Education and Training Quality Assurance body, to evaluate the accessibility of accountancy as well as chartered accountancy programmes. / Financial Accounting / M. Compt. (Applied Accountancy)

本研究目的在於探討Put-Call Parity（PCP）所隱含的買權、賣權與標的資產間的價格變動關係。藉由探討PCP偏差程度的動態行為，推論若PCP的偏差為隨機漫步過程，則無法達到長期穩定，隱含PCP的廣義關係無法成立；反之，若PCP的偏差具有回歸平均特性，表示長期會達到穩定狀態，則PCP的廣義關係成立。 在研究方法上本文以變異數比率法檢定指數選擇權的PCP偏差是否為隨機漫步過程，採用隱含利率和實際無風險利率的差代表PCP的偏差程度，利用馬可夫轉換模型描繪PCP偏差的動態行為，並使用Gibbs Sampling演算法說明參數的不確定性。 本文以S&P500和DAX為研究標的，並探討股利不確定性是否影響PCP廣義關係，得到下列結論： 1、 對於S&P 500指數選擇權而言，不論是以日資料或週資料估計VR，S&P 500的PCP偏差都無法提供回歸平均的證據，隱含S&P 500的PCP廣義關係無法成立。 2、 對於DAX指數選擇權而言，檢定日資料的結果發現，DAX之PCP偏差在長期時（40~50日）有明顯的回歸平均的證據；而在檢定週資料時，使用原始資料法在90%信心水準下，不論取任何lag都可拒絕虛無假設，使用標準化資料則無法提供明顯的回歸平均證據。 3、 比較S&P 500和DAX，檢定日資料與週資料的結果都發現，DAX的p-value都比S&P 500小，並且S&P 500的PCP偏差都無法提供回歸平均的證據，而DAX有明顯回歸平均現象，隱含在消除股利的不確定性後，指數選擇權PCP的廣義關係式成立之證據較強烈。

本論文包括3篇時間序列方法在財務的應用。第一篇以門檻向量自我迴歸模型(threshold vector autoregression)分析股市訊息傳遞的不對稱效果；第二篇利用不對稱共整合模型(asymmetric cointegration)分析中國大陸股市之間長期均衡關係；第三篇根據追蹤資料共整合檢定(panel Cointegration test)檢定購買力平價說。 第一篇文章利用門檻向量自我迴歸模型分析Nasdaq股市對台灣、日本與韓國股市不對稱的訊息傳遞效果。實證結果發現，當Nasdaq市場處於下跌狀態時（壞消息狀態），Nasdaq市場干擾對亞洲股市的衝擊較大，反之，當Nasdaq市場處於上漲狀態時（好消息狀態）時，Nasdaq市場干擾對亞洲股市的衝擊較小，而在壞消息狀態時，Nasdaq指數大跌對Jasdaq指數與Kosdaq指數的衝擊效果大於Nasdaq指數大漲的效果，Nasdaq指數小跌所產生的衝擊與小漲所產生的效果具有對稱性。 第二篇文章以Enders and Siklos(2001)不對稱共整合模型探討，中國大陸上海及深圳A股與B股股價指數之間長期不對稱的均衡關係，實證結果發現，在1992年10月至2001年8月，上海A股指數與深圳A股指數之間具有不對稱共整合關係，且當上海A股處於好消息狀態（股市上漲）時，其誤差修正項的調整速度較壞消息狀態（股市下跌）之下為快，此外，上海A股指數與深圳A股指數之間其有雙向的連動關係。在B股開放之後，則是深圳股市A股與B股指數存在不對稱共整合關係，同時Granger因果關係檢定顯示深圳B股指數領先A股指數。 第三篇文章利用Pedroni(2001)追蹤資料共整合檢定，探討大麥克漢堡價格與CPI兩種不同的價格指數用於檢定購買力平價說的有效性，根據14個國家1992-1999年的追蹤資料得到的實證結果顯示，以名目匯率作為被解釋變數，則大麥克漢堡價格與CPI都是支持PPP假說，然而若以相對價格為被解釋變數，則只有大麥克漢堡價格是支持PPP假說，而以CPI為基礎的PPP假說則是無法得到支持。除此之外，本文的實證結論並不受生產力差異的影響。 關鍵字：門檻向量自我迴歸模型、不對稱共整合、追蹤資料共整合、股票市場、購買力平價說 / This dissertation includes three financial applications using time series methods. The first article investigates the asymmetric effects of information transmissions in stock markets using threshold vector autoregression model. The second article uses asymmetric cointegration to study the long-run equilibium relationships among Chinese stock markets. The third article uses panal cointegration to test purchasing-power parity (PPP). Firstly, we examines the asymmetric effects of information transmissions of Nasdaq stock market on Taiwan, Japan, and Korea stock markets by using a threshold vector autoregressive model. And also, we check whether Nasdaq stock market have different impacts on organized stock exchanges (including TAIEX, NIKKEI 225 Index, Korea Composite Index) and over-the-counter markets (including Taisdaq Index, Jasdaq Index, and Kosdaq Index) or not. The empirical results indicate that negative innovations in Nasdaq market (bad news regime) have large influence on Asia stock markets. Particularly, the positive innovations in Nasdaq market (good news regime) have small influence on Asia stock market. The large negative innovations in Nasdaq market have great influence than those of the large positive innovations on Jasdaq Index and Kosdaq Index in bad news regime. The second article uses Enders and Sikios's (2001) asymmetric cointegration model to investigate the long-run asymmetric equihbrium relationships. The empirical results find that there exits an asymmetric cointegrated relationship between Shanghai A share index and Shenzhen A share index for the period from October 1992 to August 2001. The adjustment parameters of error correction term at Shanghai A share market are larger in bad-news regime than those in good-news regime. This result reveals investors at Shanghai possess over-reaction behavior on news of stock market. Moreover, there exists a bi-directional Granger causality between Shanghai A share index and Shenzhen A share index. We find there exists an asymmetric cointegrated relationship between Shenzhen A share index and Shenzhen B share index after 19 February 2001. Furthermore, the Shenzhen B share index leads Shenzhen A share index after 19 February 2001. The third article uses Pedroni's (2001) panel cointegration test to examine the validity of PPP hypothesis by two different price indces, i.e. Big Mac prices and CPI. Our panel observations include 14 countries from 1992 to 1999. The empirical evidence indicates Big Mac PPP and CPI PPP is supposed if we use nominal exchange rate as the explanatory variable. Nevertheless, the Big Mac PPP is valid but CPI PPP not valid if we use price level as the explanatory variable. Moveover, our concludtion does not influenced by productivity bias. Keywords: threshold vector autoregression, asymmetric cointegration, panel cointegration, stock markets, purchasing-power parity

The price level convergence of the transition economies towards the reference economies is linked to the relative price of nontradables, which is explained by the total factor productivity differentials in tradable and nontradable sector. Basic concept is offered by the Balassa Samuelson model and its modifications. Testable equations are derived from these models, and the panel data approach is applied for their estimation. The results indicate faster growth of the relative price of nontradables in transition economies as succession of higher growth rate of the total factor productivity in tradable sector. Hence estimated models confirm the price level convergence of transition economies towards the reference economies. The analyses of price dynamics of the complementary field, i. e. of the tradables, follows, and the basic concept is represented by the rational bubble hypothesis. The stress is putted on the impact of the word prices on the price levels of the Czech Republic. After a cointegration analysis of the time series is carried out, the influence of the word prices of tradable commodities is estimated within a vector error correction model and regression analysis. This cost factors analysis is afterwards related to the export dynamics of the Czech Republic, and models suitable for quantitative analysis of export dynamics as well as its prediction based on vector error correction model and regression analysis are evaluated. Their forecasting ability is assessed within a simulation of ex-post forecasts and a root mean squared error. The aim is to consider the relationship between the price levels and the export dynamics, for the relation of both variables evaluated within the Granger causality seems to be less straightforward then the standard export equations suggest, and the estimated equations confirm significant influence of the export dynamics on the price level.

Breast cancer poses a serious public health concern. This case-control study describes the relationship of night-shift working on the development of breast cancer in 57 women diagnosed with breast cancer compared to 49 women with other types of cancer in the Vaal Triangle area (selected through non-probability purposive sampling from CANSA). The study revealed that women who work night-shift developed breast cancer 1.24 times more often than women who do not work nightshift (OR=1.24 [95% CI 0.52 to 2.89]). The odds ratio was further increased in women who worked rotating-shift (OR=1.44 [95% CI 0.58 to 3.59]). Night-shift work exposure was not statistically related to the development of breast cancer. It is recommended that the relationship between night-shift exposure and breast cancer risk be further explored through cross-sectional and cohort studies, and other breast cancer pathways. / Health Studies / M. A. (Public Health)

L’industrie de la finance a connu une multiplication d’innovations qui peuvent bouleverser les services financiers traditionnels. Elles brouillent les frontières entre banques et start-ups, accélérèrent les transactions, démocratisent l'accès au crédit, tout en imposant aux régulateurs le défi de construire un cadre règlementaire qui rééquilibre le compromis entre stabilité financière, concurrence innovation.Dans cette thèse, d'abord je réponds à cette question : comment les innovations influencent-elles la concurrence dans la banque de détail ? Un premier enjeu consiste à comprendre pourquoi certains de ces services innovants sont offerts par les plateformes non-bancaires, et comment les banques peuvent rivaliser avec des participants qui appliquent un modèle d'affaire différent. Après, je regarde quels sont les facteurs d’adoption de l'innovation par les consommateurs. Pour répondre à cette question, j'étudie à l'aide d'outils d'analyse empirique l'exemple des deux principales plateformes de prêts peer-to-peer aux USA, Prosper et LendingClub. Pour terminer, je me demande si la réglementation de l'innovation est nécessaire. Est-il optimal pour la société de réglementer les fournisseurs de services innovants ? Je propose deux modèles théoriques qui s'inscrivent dans les débats bien connus sur le niveau optimal des interchanges dans les systèmes de cartes de paiement et des clauses de parité des prix et d'exclusivité sur les plateformes en ligne. / During the last years, the finance industry has experienced a proliferation of innovations which may disrupt traditional financial services. They blur the boundaries between banks and financial start-ups, speed up transactions, democratize the access to credit, revise how we can purchase goods and how merchants can sell their products, while imposing regulators the challenge for a new level playing field which balances the trade-off between financial stability, competition and innovation. In this thesis, I try to answer to three main issues related to the topic of innovation in retail banking. Firstly, how do innovations impact competition in retail banking. One first issue is to understand why some of these innovative services are offered by non-bank platforms and how can banks compete with entrants that do not have the same business model. Secondly, I look at what the drivers of the adoption of innovation by consumers in retail banking are. What determines the diffusion of a new financial technology despite all the financial risks related to it ? To answer to these questions, I will look empirically at the example of the two main peer-to-peer lending platforms in the USA, Prosper and LendingClub. Third, I address the question on whether regulation of innovation is necessary. Is it optimal for the society to regulate the providers of innovative retail banking services? To answer to these questions, I address, in two theoretical models, the well-known debates on the optimal level of interchange fees in payment card systems and the imposition of exclusivity arrangements and price parity clauses in contracts between platforms and merchants.