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Yes / Angiography is a minimally invasive diagnostic procedure in endovascular interventions. Training interventional procedures is a big challenge, due to the complexity of the procedures with the changes of measurement and visualization in blood flow rate, volume, and image contrast. In this paper, we present a novel virtual reality-based 3D interactive training platform for angiography procedure training. We propose a multi-fluid flow approach with a novel corresponding non-slip boundary condition to simulate the effect of diffusion between the blood and contrast media. A novel syringe device tool is also designed as an add-on hardware to the 3D software simulation system to model haptics through real physical interactions to enhance the realism of the simulation-based training. Experimental results show that the system can simulate realistic blood flow in complex blood vessel structures. The results are validated by visual comparisons between real angiography images and simulations. By combining the proposed software and hardware, our system is applicable and scalable to many interventional radiology procedures. Finally, we have tested the system with clinicians to assess its efficacy for virtual reality-based medical training. / National Natural Science Foundation of China grant number 61402278, the Shanghai Natural Science Foundation of China grant number 14ZR1415800, Research Program of Shanghai Engineering Research Center of Motion Picture Special Effects grant number 16dz2251300, Shanghai University Film Peak Discipline, and Shanxi Natural Science Technology Foundation grant number 2016JZ026.

Stroke is a leading cause of morbidity and long-term neurological disability in the U.S. Ischemic stroke, which accounts for approximately 90% of all strokes, is the result of an occlusion in the arteriole cerebrovascular network. No effective treatment options exist to provide neuroprotection from occlusion, and limited success has been seen clinically when attempting to restore blood flow to vulnerable neural tissue regions. Enhancement of pial collateral remodeling (Arteriogenesis) has recently been shown to improve blood flow and mitigate neural tissue damage following stroke (1-3). Arteriogenesis is the remodeling of pre-existing arteriole vessel which are able to re-route blood to blood-deprived regions of tissue. Arteriogenesis requires endothelial cell (EC) and smooth muscle cell proliferation, extracellular matrix degradation and recruitment of circulating bone marrow-derived cells (4-6). Unlike spouting angiogenesis, which requires weeks following occlusion to develop, arteriogenesis begins as early as 24-48hrs post-stroke (7, 8) and can expeditiously enhance blood flow to ischemic regions, making it an attractive target for therapeutic intervention. Our preliminary studies, in an EphA4 global knockout mouse model, indicated that EphA4 receptor tyrosine kinase severely limits pial arteriole collateral formation. The preliminary work also showed that activation of EC EphA4 receptor in vitro inhibited vascular formation. Additionally, ECs lining the collateral vessel have been shown to play a role in collateral remodeling (9). Taken together, the objective of this dissertation was to elucidate the cell autonomous role of the EphA4 receptor and given the central role of the EC in collateral remodeling, we postulated that EphA4 receptor on ECs the limits pial collateral formations. Using a cell-specific loss-of-function approach, we tested the hypothesis that EC-specific EphA4 plays an important role in pial collateral development and remodeling after induced stroke. The results from this dissertation show that (1) EphA4 expression on ECs suppress the formation of pial collaterals during development and limits EC growth via suppression of p-Akt in vitro (2) EC-specific EphA4 ablation leads to increased collateral remodeling, enhanced blood flow recovery, tissue protection and improved neurological behavioral outcomes after stroke and (3) Mechanistically, EphA4 limits pial collateral remodeling via attenuation of the Tie2/Angiopoietin-2 signaling pathway. The work presented in this dissertation demonstrate that EphA4 can be targeted therapeutically to increase pial collateral remodeling to alleviate neurological deficits after ischemic stroke. / Doctor of Philosophy / Stroke is the fifth leading cause of death in the United States. Ischemic stroke is the most common type of stroke and occurs when blood flow to part of the brain is impeded. Lack of blood results in cell death and tissue damage in the brain. In an effort to restore blood flow, specialized blood vessels in the brain called collaterals remodel and become larger to allow re-routed blood to the blood-deprived region of the brain. The duration it takes to remodel these remarkable blood vessels and re-route blood varies in humans, and sometimes is not able to prevent adequate tissue damage. The current work explores novel therapeutic targets to accelerate collateral remodeling in an effort to reduce tissue loss after stroke. We present studies which show that a protein called EphA4, found on endothelial cells restricts remodeling, and when inhibited in the brain can increase collateral remodeling and reduced adverse effects after ischemic stroke.

An experimental investigation was done on oxygen transfer into a steady, laminar flow of whole blood and hemoglobin solutions. The effects of facilitation and augmentation on the bulk transfer were studied. The transfer problem was modeled numerically and effective diffusivities were calculated for all of the experiments. Significant increases in transfer due to both facilitation and augmentation were observed. Ghost cells were found to have no effect on transfer into hemoglobin solutions. / Master of Science

Continuous-wave (CW) Doppler echocardiographic responses to passive tilting were measured in 39 men using the following protocol: standing; supine; +20° head-up; supine; â 20° head-down. Twenty of the subjects were normotensive (NTN) and the rest were borderline hypertensive (B-HTN) according to prior medical diagnosis. Doppler recordings of blood flow for aortic peak velocity (Pkv), peak acceleration (PkA), and stroke velocity integral (SVI) were taken after 15 minutes in each posture. A skilled technician, using the measurement procedures recommended by the instrument manufacturer, positioned the handâ he1d probe at the supra-sternal notch during recording. For both NTN and Bâ HTN groups, Pkv and PkA were unaffected by the imposed postural changes. The SVI was significantly altered (P<0.05) by postural stress, with the NTN group generally showing greater changes than the Bâ HTNs. The standing-to-supine postural change was associated with the largest change in SVI: NTN = 8.0 to 10.7 cm (+34%) and B-HTN = 7.6 to 8.8 cm (+15%). These results were interpreted as follows (1) SVI appears to be sensitive to changes in ventricular pre-load, while PkA and Pkv are not; (2) SVI changes with passive tilting follow the patterns expected for change in ventricular stroke volume and; (3) attenuated SVI responses to postural tilting may suggest impairment in cardiovascular regulation peculiar to individuals at risk for hypertension. / Master of Science

Ketone monoester (KME) supplements are one exogenous ketone intervention which has demonstrated benefits to multiple facets of brain health, including cerebral blood flow (CBF) and cognition. However, it is unknown how KME impact CBF and cognition acutely, and whether the size of KME dose differentially impacts these outcomes. Higher KME doses lower blood pH and arterial CO2 (PaCO2), which are important regulators of CBF. We hypothesized that high-dose KME ingestion would lower CBF via acidosis-induced compensatory reductions in PaCO2, whereas low-dose KME ingestion would enhance CBF, mirroring past findings from other exogenous ketone interventions. Changes in cognitive function were also hypothesized to parallel CBF responses. Twenty young adults (age=23±3 years; BMI=23.4±2.2 kg/m2) participated. In a double-blinded, counterbalanced, crossover design, participants completed 3 separate conditions: 1) high-dose KME (0.6 g/kg); 2) low-dose KME (0.3 g/kg); or 3) placebo. Outcome measures were assessed at fasting baseline, 45-, and 120-min post-ingestion. CBF was assessed using Duplex ultrasound of the internal carotid and vertebral arteries. End-tidal CO2 (PETCO2) was measured using a gas analyzer, to approximate PaCO2. Hippocampal-dependent function was assessed using the lure discrimination index (LDI) and recognition memory score (REC) from the mnemonic similarity task. Over a 2-hour period post-ingestion, low- and high-dose KME lowered CBF to a different extent relative to baseline (45-min (low-dose, high-dose): ∆10.4%, ∆14.0%; 120-min (low-dose, high-dose): ∆6.2%, ∆18.6%; P < 0.001). These reductions were mirrored by dose-dependent reductions in PETCO2 and changes in CBF were positively correlated with changes in PETCO2 (P < 0.001, R2 = 0.219). Despite reductions in CBF, both LDI (P = 0.619) and REC (P = 0.651) were unchanged in the KME conditions. These findings provide a foundational characterization of the acute effects of KME dose on CBF and cognition, which will inform potential therapeutic recommendations on KME for brain health. / Thesis / Master of Science (MSc) / In addition to being an alternative energy source used during fasting or when consuming low amounts of carbohydrates, ketone bodies may act as signals that impact various aspects of brain health. Recent studies suggest that supplementating with a drink that contains ketones is an alternative way to increase ketones in your blood, without dietary modifications. We investigated whether one-time ingestion of a ketone supplement (KME) affects brain blood flow and cognition, as well as whether the size of KME dose differentially impacts these outcomes. Our results show that KME ingestion lowers brain blood flow, to a different extent depending on the dose that was ingested. Despite this, there was no change in memory performance from taking this ketone supplement. These findings were important in demonstrating how KME ingestion impacts the brain, and will inform future guidelines on its potential use for protecting and/or improving brain health.

It was generally accepted that the rate of formation of cerebrospinal °uid (CSF) is independent of intraventricular pressure [26], until A. Sahar and a host of other scientists challenged this belief. A. Sahar substantiated his belief that the rate of (CSF) formation actually depends on intraventricular pressure, see A. Sahar, 1971 [26]. In this work we show that CSF formation depends on some other factors, including the intraventricular pressure. For the purpose of this study, we used the capillary blood °ow model proposed by K.Boryczko et. al., [5] in which blood °ow in the microvessels was modeled as a two-phase °ow; the solid and the liquid volume phase. CSF is formed from the blood plasma [23] which we assume to be in the liquid volume phase. CSF is a Newtonian °uid [2, 23]. The principles and methods of e®ective area" developed by N. Sauer and R. Maritz [21] for studying the penetration of °uid into permeable walls was used to investigate the ¯ltrate momentum °ux from the intracranial capillary wall through the pia mater and epithelial layer of the choroid plexus into the subarachnoid space. We coupled the dynamic boundary equation with the Navier-Stoke's constitutive equation for incompressible °uid, representing the °uid °ow in the liquid volume phase in the capillary to arrive at our model. / Mathematical sciences / M.Sc.

Submitted in partial compliance with the requirements for the Master’s Degree in Technology: Chiropractic, Durban University of Technology, Durban, South Africa, 2015. / Background: When a soft tissue injury occurs the blood vessels and surrounding tissue are damaged leading to haemorrhaging and inflammation. Cryotherapy (cold therapy) is generally acknowledged as the preferable treatment by manual therapists during this immediate post-traumatic period of an injury. Cryotherapy has been shown to result in vasoconstriction decreasing the rate of blood flow which has a favourable effect on inflammation and pain. The commercially available cooling cuff is a relatively new cryotherapy modality offering a mechanism of cooling that does not require freezing and is easy to use. The polymer granules within the cooling cuff are activated by emersion in water therefore freezing is not required making the cooling cuff readily available compared to more traditional forms of cryotherapy. Aim: The aim of this study was to determine the effect of a moist ice pack and a commercially available cooling cuff radial artery blood flow (cm.s-1) and radial artery lumen diameter (mm) after 15 minutes of application. Method: This study was a pre-test post-test design utilising 43 asymptomatic participants that were randomly allocated to one of two groups. Each group either received a standard moist ice pack or a commercially available cooling cuff, placed on the ventral surface of the participants forearm, over the radial artery, for a duration of 15 minutes. Measurements were taken with a Doppler ultrasound to determine radial artery blood flow and lumen diameter, prior to the intervention and 15 minutes after the cryotherapy application. Data analysis was performed using IBM SPSS VERSION 20 (IBM Corp. Released 2010.IBM SPSS Statistics for Windows, Version 19.0. Armonk, New York: IBM Corp.). Statistical significance was set at a p< 0.05 level. Intra-group and inter-group comparisons were measured using repeated measures ANOVA testing. Results: Both the moist ice pack and commercially available cooling cuff resulted in a significant decrease in radial artery blood flow (p< 0.001) after 15 minutes of application with no significant changes being observed in radial artery diameter Conclusions: The commercially available cooling cuff resulted in a similar effect on radial artery blood flow and lumen diameter as moist ice, indicating that the commercially available cooling cuff may be utilised in the acute phase of an injury to alter blood flow. / M