Financial intermediaries are paramount for modern society. During the last decade, however, our reliance on these institutions have been meticulously debated, especially in the aftermath of the financial crisis. This thesis contributes to this debate with a novel perspective on loan supply changes in light of the recent events in the Swedish real estate market. More specifically, it investigates what influence housing prices have on the supply of commercial and industrial loans. This is done by estimating dynamic panel data models using a quarterly panel containing balance sheet data for 68 Swedish monetary financial institutions, during the post-financial crisis period of 2009-2017. The results indicate that housing prices do not have a significant effect on commercial and industrial loan supply. However, these loans are to a considerable degree dependent on the institutes’ earlier levels of commercial and industrial loans.

Peripheral arterial occlusive disease (PAOD) often presents as intermittent claudication, which may be caused by impaired vasodilation. Impairment of resistance vessels may contribute to the pathogenesis of PAOD, and explain the poor correlation between resting blood flow and limb function. Collateral function following arterial occlusion is not well defined, however collaterals and arterialized collateral capillaries (ACCs) in male and female animal models exhibit impaired vasodilation following arterial occlusion, which can potentially be improved with exercise training. Furthermore, resistance vessels in the ischemic tree and stem are likely involved in the pathogenesis of PAOD, however the relative importance of each is unknown. Therefore, we measured functional vasodilation in pre-existing collaterals, ACCs, the ischemic tree, and the stem region, 7 and 21-days following spinotrapezius feed artery ligation in male and female BALB/c mice, and with exercise therapy. Vasodilation in ACCs was more impaired in female mice than in males. Generally, vasodilation was impaired at day-7, likely due to impaired endothelium-dependent and smooth muscle-dependent vasodilation in maturing collaterals, and recovered by day-21. Exercise training appears to enhance collateral reactivity, more in ACCs in males than in females, suggesting that its therapeutic benefits are linked not only to structural adaptation but also to vessel functionality. Therefore, future research is required to determine the cause of sex differences in exercise therapy to treat peripheral arterial occlusive disease.

Peripheral arterial occlusive disease (PAOD) is characterized by buildup of atherosclerotic plaque in peripheral arteries that leads to an occlusion that can interrupt the supply of blood to the peripheral tissue, causing downstream tissue ischemia/hypoxia. PAOD is estimated to affect over 200 million patients worldwide. Current surgical revascularization treatments can be effective in about half of the patient population, leading to a significant number of patients with no treatment options beyond pharmacological intervention and lifestyle modification. The decrease in blood flow downstream of the occlusion leads to increased blood pressure gradient in the microvasculature, specifically in vessels that connect arterial trees (known as collaterals), which will structurally enlarge and increase blood flow to the downstream ischemic/hypoxic tissue. Targeting this process, known as arteriogenesis, can provide a potential treatment option for patients suffering from PAOD by redirecting blood flow around an occluded artery and therefore supplying hypoxic tissue with blood. In order to enhance this process, cellular transplantation has been used but the current cell types explored have not been successful in enhancing arteriogenesis. Myoblasts, proliferative muscle progenitor cells, mediate muscle regeneration, and promote angiogenesis (the growth of new capillaries to supply hypoxic tissue). Preliminary data indicates that myoblasts also promote arteriogenesis in obese mice, making them an attractive therapeutic candidate. However, the methods used in the preliminary studies limited our ability to confirm those findings and characterize the cell therapy candidate. Specifically, we lacked a reproducible and optimized method to isolate myogenic cells and characterize these cells during in vitro culture and after in vivo transplantation. Therefore, the 1st Aim of this study was to optimize the isolation to obtain the highest number possible of satellite cell-yielding myofibers by modification of enzymatic and mechanical digestion of extensor digitorum longus muscle. Modifications to this methodology increased myofiber yield by more than 150%. The 2nd Aim was to optimize the expansion of satellite cell-derived myoblasts by modification of culture media supplements to promote cell expansion while minimizing maturation. bFGF and SB 203580 supplementation improved cell proliferation and prevented myogenic cell maturation during 7-days of in vitro culture. The 3rd Aim was to develop a process for evaluating the quantity and identity of isolated myogenic cells before and after transplantation. This was achieved by implementing an immunofluorescent transcription factor labeling protocol to determine cell identity and a live/dead cell viability assay to determine cell viability and quantity. All 3 aims were integrated into a proof-of-concept pilot study on a hindlimb ischemic BALB/c mouse model. While myoblast transplantation failed to increase collateral arteriogenesis in this model, the process developed in this project provides a reproducible framework for future studies on myoblast-enhanced arteriogenesis. Further research on the effects of myoblast transplantation on arteriogenesis may facilitate the development of new therapies that improve the prognosis of patients with PAOD.

This thesis examines the transmission of monetary policy and the effects of persistent cost-push shocks in the presence of high household indebtedness (DTI) and frictions in fixed-rate mortgage (FRM) interest rates. A dynamic stochastic general equilibrium (DSGE) model incorporating housing, household debt, and long-term FRMs is estimated to accomplish this. The key findings can be summarized as follows: (i) A higher DTI leads to a stronger transmission of monetary policy, although this effect is dampened by the degree of interest rate fixation periods. (ii) Cost-push shocks propagates more strongly to inflation when the interest rate fixation periods is longer, resulting in delayed and slightly muted effects on output and consumption compared to adjustable-rate mortgages (ARM). (iii) While stronger responses to inflation help mitigate the cost-push shock, this comes at the expense of a larger output gap but with a slightly faster stabilization of the economy with a somewhat steeper recovery.

Indiana University-Purdue University Indianapolis (IUPUI) / Collateral connections in the brain, also known as Leptomeningeal Anastomoses, are connections between blood vessels originating from different arteries. Despite limited knowledge, they are suggested as an important contributor to cerebral stroke recovery that allows additional blood flow through the affected area. However, few databases and algorithms exist for this specific task of locating them. In this paper, a MATLAB program is developed to find these connections and detect strokes to replace manual labeling by professionals. The limited data available for this study are 23 2D microscopy images of mice cerebral vascular structures highlighted by dyes. In the images, strokes are shown to diminish the pixel count of vessels below 80\% compared to the healthy brain. Stroke classification error is greatly reduced by narrowing the scope from comparing the entire hemisphere to one smaller region. A novel way of finding collateral connections is utilizing connected components. Connected components organize all adjacent pixels into a group. All collateral connections can be found on the border of two neighboring arterial flow regions, and belong to the same group of connected components with the arterial source from each side. Along with finding collateral connections, a newly created coordinate system allows regions to be defined relative to the brain landmarks, based on the brain's center, orientation, and scale. The method newly proposed in this paper combines stroke detection, brain coordinate system extraction, and collateral connection detection in stroke-affected mouse brains using only image processing techniques. This allows a simpler, more explainable result on limited data than other techniques such as supervised machine learning. In addition, the new method does not require ground truth and high image count for training. This automated process was successfully interpreted by medical experts, which allows for further research into automating collateral connection detection in 3D.

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Stroke, a life-threatening condition, primarily resulting from ischemic events often caused by occlusion of the middle cerebral artery (MCA). Pre-existing leptomeningeal collateral (LMC) vessels connect MCA branches to anterior or posterior arteries, situated along the brain's cortical surface or meninges, under healthy conditions these vessels remain dormant due to their small diameters and relatively low flow velocity. LMCs serve as vascular redundancies that retrogradely re-supply blood to help salvage the penumbra following cerebral vascular occlusion. Their outward growth or remodeling (arteriogenesis) is essential for promoting cerebral reperfusion and preventing tissue damage after ischemic stroke. Increased fluid shear stress on collateral vessel wall activates arteriogenesis result in the activation of the endothelium and subsequent recruitment of peripheral-derived immune cells (PDICs), which have been shown to aid this unique adaptive process in other organ systems, however their role and mechanism(s) involved in LMC remodeling in stroke has not previously been evaluated. Initial findings suggest the EphA4, a well-established axonal growth and guidance receptors, plays a novel role in LMC arteriogenesis. This dissertation examined PDIC-specific functions of EphA4 using GFP labeled bone marrow chimeric mice subjected to permanent middle cerebral artery occlusion (pMCAO). We assessed immune cell population changes, infarct volume, functional recovery, characterized subtypes of infiltrated immune cell, and measured collateral vessel diameters. Additionally, we explored the Tie2-mediated PI3K signaling pathway in peripheral-derived monocyte/macrophages (PDM) treated with soluble Tie2-Fc and a PI3K p110α inhibitor. The results from this dissertation show that loss of PDIC-specific EphA4 led to increased collateral remodeling, associated with decreased infarct volume, improved cerebral blood flow, and functional recovery within 24 hours post-pMCAO. The crosstalk between EphA4-Tie2 signaling in PDMs, regulated through PI3K/Akt axis, inhibited pial collateral remodeling. In conclusion, our findings highlight the negative regulatory role of PDM-specific EphA4 in collateral growth and remodeling by inhibiting Tie2 function via the PI3K regulated pathway. Peripheral myeloid-derived EphA4 emerges as a new regulator of cerebral vascular injury and neuroinflammation following acute ischemic stroke. / Doctor of Philosophy / Stroke, a life-threatening condition, occurs when blood flow to part of the brain is disrupted due to the vascular occlusion of a major brain artery, such as the MCA. Within protective layers of our brain, there are pre-existing pial collateral vessels that act as backup connections. These vessels play an important role in increasing cerebral reperfusion and preventing tissue damage after stroke. One fascinating aspect of stroke recovery involves PDICs. These immune cells migrate into the blood hypo-perfused region of the brain and regulate the growth of collateral vessels. However, the specific functions of PDICs, particularly a receptor called EphA4, has remained unclear. Our research delved into the immune response following ischemic stroke using genetically modified mice. We examined immune cell populations, infarct volume (the damaged brain tissue), functional recovery, and collateral vessel diameters. Notably, we discovered that deletion of PDIC-specific EphA4 enhanced collateral vessel remodeling. This led to decreased infarct volume, better blood flow, and improved functional recovery within 24 hours after stroke. Furthermore, we explored a signaling pathway involving Tie2 and PI3K in PDM. This crosstalk between EphA4 and Tie2, mediated through PI3K regulation, played a critical role in suppressing collateral vessel remodeling. In summary, understanding how immune cells contribute to stroke recovery may pave the way for novel therapeutic approaches to enhance outcomes for stroke patients.