Systemic risk in the financial sector; a review and synthesis

In a financial crisis, an initial shock gets amplified while it propagates to other financial intermediaries, ultimately disrupting the financial sector. We review the literature on such amplification mechanisms, which create externalities from risk taking. We distinguish between two classes of mechanisms: contagion within the financial sector and pro-cyclical connection between the financial sector and the real economy. Regulation can diminish systemic risk by reducing these externalities. However, regulation of systemic risk faces several problems. First, systemic risk and its costs are difficult to quantify. Second, banks have strong incentives to evade regulation meant to reduce systemic risk. Third, regulators are prone to forbearance. Finally, the inability of governments to commit not to bail out systemic institutions creates moral hazard and reduces the market’s incentive to price systemic risk. Strengthening market discipline can play an important role in addressing these problems, because it reduces the scope for regulatory forbearance, does not rely on complex information requirements, and is difficult to manipulate.

Banking risk and regulation: Does one size fit all?

Using data for more than 200 banks from 21 OECD countries for the period 2002 to 2008, we examine the impact of bank regulation and supervision on banking risk. Supervisory control, and regulations on capital and market entry have a significant impact on 'capital and asset risk', while supervisory control and regulations on activities restrictions, private monitoring, market entry, and liquidity, have a significant effect on 'liquidity and market risk'. However, quantile regressions suggest that the effect of regulation and supervision differs across banks: most indicators of bank regulation and supervision do not have a significant effect on low-risk banks, while they do affect high-risk banks.

The relationship between high/low birth weights and future development of diabetes mellitus among aboriginal people : a case-control study using Saskatchewan's health data systems

In recent decades, rates of type 2 diabetes mellitus (T2DM) and diabetic complications have reached epidemic proportions among Canadian Aboriginal people. Evidence in several populations suggests that abnormal birth weight, particularly low birth weight (LBW) and possibly high birth weight (HBW) may be linked to the development of T2DM. LBW often reflects poor maternal health/ nutritional status which may interfere with normal pancreatic development. HBW is a frequent complication of diabetic pregnancies which are associated with obesity and carbohydrate intolerance in adulthood. Since Saskatchewan Aboriginal newborns historically had higher rates of LBW, and more recently have experienced higher HBW rates, it follows that sub-optimal maternal/ fetal health may be important in the epidemic of T2DM in this population. This thesis describes a case-control study that used Saskatchewan Health databases to determine the relationship between birth weight and T2DM. A sample of 846 adult diabetic Registered Indians (RI) were age and sex matched to three control groups: 1) non-diabetic RI, 2) diabetic general population (GP) subjects, and 3) non-diabetic GP subjects. RI subjects were identified as such by the provincial Health Insurance Registration File. The results of this study show a significant association between HBW (> 4000 grams) and T2DM for RI people [odds ratio (OR) 1.63; 95% confidence interval (CI) 1.20, 2.24]. This association increased in strength from the middle to the latter part of this century and was found to be stronger for RI females than RI males. The comparison of birth weights within the four study groups revealed that diabetic RI (16.2%) were significantly more likely (

Epigenetic regulation of somatostatin receptors in neuroendocrine tumors:A Novel Therapeutic Approach?

The overexpression of somatostatin type-2 receptors (SSTR2) on neuroendocrine tumor (NET) cells forms a pivotal biomarker for theranostic approaches. Radiolabeled somatostatin analogues (SSAs), most frequently [68Ga]Ga-DOTATATE and [177Lu]Lu-DOTATATE for nuclear imaging and therapy, respectively, have shown to be of great importance for NET disease management. [177Lu]Lu-DOTATATE treatment, known as peptide receptor radionuclide therapy (PRRT), is EMA and FDA approved for unresectable or metastatic, progressive, well-differentiated SSTR2-positive gastroenteropancreatic NET patients. However, complete responses after therapy are rare and progressive disease is often observed. Approaches to further improve PRRT efficacy are thus of great need. The aim of the studies described in this thesis is to upregulate SSTR2 on NET cells by modulating the epigenetic machinery, in order to increase radiolabeled SSA uptake and ultimately improve treatment response. Furthermore, we aimed to gain more insights into the interaction between epigenetic marks and the regulation of SSTR2 expression. Our studies were performed preclinically using different NET cell lines. In addition to in vitro studies with these cell lines, mice with tumors derived from these cell lines and NET patient tissue samples were used. Furthermore, the effect of epigenetic drugs on the uptake of [68Ga]Ga-DOTATATE was investigated in NET patients

Epigenetic regulation of somatostatin receptors in neuroendocrine tumors:A Novel Therapeutic Approach?

The overexpression of somatostatin type-2 receptors (SSTR2) on neuroendocrine tumor (NET) cells forms a pivotal biomarker for theranostic approaches. Radiolabeled somatostatin analogues (SSAs), most frequently [68Ga]Ga-DOTATATE and [177Lu]Lu-DOTATATE for nuclear imaging and therapy, respectively, have shown to be of great importance for NET disease management. [177Lu]Lu-DOTATATE treatment, known as peptide receptor radionuclide therapy (PRRT), is EMA and FDA approved for unresectable or metastatic, progressive, well-differentiated SSTR2-positive gastroenteropancreatic NET patients. However, complete responses after therapy are rare and progressive disease is often observed. Approaches to further improve PRRT efficacy are thus of great need. The aim of the studies described in this thesis is to upregulate SSTR2 on NET cells by modulating the epigenetic machinery, in order to increase radiolabeled SSA uptake and ultimately improve treatment response. Furthermore, we aimed to gain more insights into the interaction between epigenetic marks and the regulation of SSTR2 expression. Our studies were performed preclinically using different NET cell lines. In addition to in vitro studies with these cell lines, mice with tumors derived from these cell lines and NET patient tissue samples were used. Furthermore, the effect of epigenetic drugs on the uptake of [68Ga]Ga-DOTATATE was investigated in NET patients

The relationship between Dispositional Optimism, Pain Experience and Pain anticipation

Background: Dispositional optimism is an individual difference variable that reflects the extent to which people hold generalized favorable expectancies for their future. It has been suggested to be a protective factor for pain. This study investigates the relationship between dispositional optimism and pain experience, and what role pain anticipation plays in this relationship. A positive impact of dispositional optimism on pain experience is expected. Furthermore, it is expected that pain anticipation has a negative association with both dispositional optimism and pain experience, but also may be a mediator in the relationship between dispositional optimism and pain experience. Methods: The study has a cross-sectional design and was performed on 36 bachelor students of Maastricht University. The study population has an age ranged from 18 to 24 years old (mean= 20,75 years; SD= 1,84). Experimental pain was induced by means of the Medoc Pathway Advanced Thermal Stimulator (ATS; MEDOC). Pain experience was separated in pain threshold and pain tolerance measurements. Dispositional optimism was measured with the Life Orientation Test-Revised (LOT-R). Pain anticipation was separated in three items; expected pain, expected unpleasantness, and expected fear, which were measured on a visual analogue scale before the start of the pain stimulus. Results: For pain anticipation and pain experience only expected pain shows a significant correlation with pain experience’s measurement pain tolerance. There is no significant link between dispositional optimism and pain experience; therefore, pain anticipation is not tested as a mediator. In the correlation between pain anticipation and dispositional optimism, the link between expected pain and the total LOT-R score is significant. Furthermore, the links between expected pain, expected unpleasantness and expected fear and the negative subscale of the LOT-R score are significant. Conclusion: This study did not confirm the suggested relationship between dispositional optimism and pain experience, although it does confirm a significant correlation between pain anticipation and dispositional optimism