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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