In the dissertation are analyzing the main characteristics of asphalt concrete influencing shear deformation, appearance and increase of rutting connected with them, analyze the influence of geosynthetic material characteristics onto asphalt concrete functioning.

The behavior of unsaturated soils depends heavily on material properties and soil conditions. In Geotechnical Engineering, compacted soils are frequently used as fill material, and quality control is vital to the construction process. There are few methods available to estimate the parameters associated with unsaturated soils based on field measurements, and a relationship between these factors could reduce testing time and lower construction costs. Undrained triaxial tests were performed on four clays representing a range of material properties in an effort to reach the maximum dry density, which provides the highest bearing capacity. Each clay was compacted at optimum moisture content, as well as wet and dry of optimum. Measurements were taken using the GeoGauge and shear wave velocities. An empirical approach was used to estimate the effect of a density gradient on soil suction. A relationship between the normal stress and matric suction produced a strong trend when plotted against a function of stiffness and the void ratio, which represents a density gradient. Another relationship between the GeoGauge and shear wave stiffness measurements was found, but no relationship with the material properties of the samples was observed, indicating that more in-depth research is needed to find a stronger relationship.

The use of fibre reinforced polymer (FRP) composites as an alternate to steel has proved to be an effective solution to the corrosion problem. However, FRP bars have low axial and transverse stiffness compared to steel bars which results in a lower shear capacity of FRP reinforced concrete (RC) elements compared to steel-RC elements. Flat plate systems are commonly used to take advantages of the absence of beams. They, however, are susceptible to punching shear failure where the column suddenly punches through the slab. An experimental program was conducted to investigate the punching shear behaviour of slab-column edge connections. Nine isolated full-scale slab-column edge connections were constructed and tested to failure. One connection was reinforced with steel flexural reinforcement, six with GFRP flexural reinforcement and two with GFRP flexural and shear reinforcement. The parameters investigated were the flexural reinforcement type and ratio, the moment-to-shear ratio and the shear reinforcement spacing.

Experiments were performed to examine the shear resistance of heavily reinforced I-beams. Six I-beams with identical cross sections were constructed using high strength self-consolidating concrete, and were tested under monotonic anti-symmetric loading. All specimens had almost the same amount of longitudinal reinforcement, which provided sufficient flexural capacities. There were two variables: shear span and shear reinforcement ratio. Test results showed that ACI code was too conservative in predicting the shear strengths of heavily shear reinforced I-beams, and the shear strength limit for deep beams should be increased to account for the benefit of high strength concrete. However, doubling the amount of stirrups did not improve the ultimate shear resistance much. The three beams that contained around 2.45% stirrups showed over-reinforced shear failures. Longitudinal flange cracking occurred to every specimen due to lack of cross tie reinforcement in the flanges, and it was believed to have reduced the ultimate shear strength.

Experiments were performed to examine the shear resistance of heavily reinforced I-beams. Six I-beams with identical cross sections were constructed using high strength self-consolidating concrete, and were tested under monotonic anti-symmetric loading. All specimens had almost the same amount of longitudinal reinforcement, which provided sufficient flexural capacities. There were two variables: shear span and shear reinforcement ratio. Test results showed that ACI code was too conservative in predicting the shear strengths of heavily shear reinforced I-beams, and the shear strength limit for deep beams should be increased to account for the benefit of high strength concrete. However, doubling the amount of stirrups did not improve the ultimate shear resistance much. The three beams that contained around 2.45% stirrups showed over-reinforced shear failures. Longitudinal flange cracking occurred to every specimen due to lack of cross tie reinforcement in the flanges, and it was believed to have reduced the ultimate shear strength.

The purpose of this study is to model and analyze the nonplanar shear wall assemblies of shear wall-frame structures. Two three dimensional models, for open and closed section shear wall assemblies, are developed. These models are based on conventional wide column analogy, in which a planar shear wall is replaced by an idealized frame structure consisting of a column and rigid beams located at floor levels. The rigid diaphragm floor assumption, which is widely used in the analysis of multistorey building structures, is also taken into consideration. The connections of the rigid beams are released against torsion in the model proposed for open section shear walls. For modelling closed section shear walls, in addition to this the torsional stiffness of the wide columns are adjusted by using a series of equations. Several shear wall-frame systems having different shapes of nonplanar shear wall assemblies are analyzed by static lateral load, response spectrum and time history methods where the proposed methods are used. The results of these analyses are compared with the results obtained by using common shear wall modelling techniques.

Endothelial cells (EC) exposed to oscillatory shear stress (OS) experience oxidative stress as a signature of atherosclerosis. Conversely, unidirectional laminar shear stress (LS) reduces reactive oxygen species (ROS) levels and inflammatory responses. Peroxiredoxins (PRX) are antioxidant enzymes that reduce hydrogen peroxide, but have yet to be investigated in response to shear stress. We hypothesized that LS, compared to OS, promotes increased expression of PRX, which in turn influences the balance of ROS in EC. In this study, we identified all six PRX family members in bovine aortic endothelial cells (BAEC). Furthermore, we revealed that PRX are regulated by shear stress in EC. When compared to OS and static culture (ST), exposure to chronic LS upregulated PRX1 levels intracellularly. LS also upregulated PRX5 relative to ST, but not OS. In addition, PRX exhibited broad subcellular localization in BAEC, but these patterns did not change in response to shear stress. To establish the functional importance of PRX1 in shear stress-dependent redox balance, we next examined the role of PRX1 in LS-mediated hydrogen peroxide regulation. Here, Amplex Red assay was used to measure ROS levels in BAEC. Depletion of PRX1 using siRNA resulted in significantly higher ROS levels following LS, OS, and ST, while PRX5 depletion did not. These findings indicated that chronic exposure to LS upregulates PRX1 expression to keep ROS levels low in EC. To identify the pathway by which atheroprotective LS stimulates PRX1 protein production, we also undertook gene expression studies. We discovered that LS upregulates Prdx1 gene in a time-dependent manner compared to OS or ST. However, this increase in expression was not due to stabilization of Prdx1 mRNA. In addition, Prdx1 promoter analysis revealed a Nrf2 transcription factor binding site 160bp upstream of the gene. Nrf2 overexpression promoted basal PRX1 protein production, while Nrf2 depletion reduced Prdx1 mRNA following exposure to LS. Collectively, our work illustrated that LS affects PRX1 by inducing the Prdx1 gene, in part via the transcription factor Nrf2. Moreover, this discovery of PRX1 as a mechanosensitive antioxidant may contribute important insights into endothelial cell biology and provide a novel therapeutic target for vascular diseases.

Atherosclerosis occurs preferentially at branches and curves in arteries exposed to disturbed flow while sparing straight portions of arteries exposed to undisturbed flow. In vivo and in vitro studies have implicated NADPH oxidases in atherosclerosis and hypertension. Shear stress can induce reactive oxygen species production in endothelial cells from a variety of sources, including NADPH oxidases. Here, we examined the hypothesis that unidirectional laminar shear (LS) and oscillatory shear (OS) would differentially regulate gene expression profiles in NADPH oxidase-dependent and -independent manners, and that these genes would provide novel molecular targets in understanding endothelial cell biology and vascular disease. The p47phox subunit of the NADPH oxidase can be an important regulator of certain Nox isoforms, including Nox1 and Nox2 which may be responsible for shear-induced superoxide production. In order to isolate p47phox-dependent shear responses, we took advantage of the p47phox-/- transgenic mouse model which lacks a functional p47phox subunit. We developed a method to isolate murine aortic endothelial cells using an enzymatic digestion technique. These cells expressed characteristic endothelial markers, including VE-cadherin, PECAM1, and eNOS, and aligned in the direction of flow. We successfully isolated primary murine aortic endothelial cells from both wild-type C57BL/6 mice (MAE-WT) and p47phox-/- mice (MAE-p47). Furthermore, we established an immortalized cell line from each of these cell types, iMAE-WT and iMAE-p47. We carried out microarray studies using Affymetrix Mouse Genome 430 2.0 Arrays (39,000+ transcripts) on MAE-WT and MAE-p47 that were exposed to atheroprotective LS or atherogenic OS for 24 hours. In comparison to LS, OS significantly changed the expression of 187 and 298 genes in MAE-WT and MAE-p47, respectively. Of those, 23 genes showed similar gene expression patterns in both cell types while 462 genes showed different gene expression patterns in the two cell types, demonstrating a considerable role for p47phox-based NADPH oxidases in shear-dependent gene expression. Changes in expression of several genes, including Kruppel-like factor 2 (Klf2), endothelial nitric oxide synthase (eNOS), angiopoietin 2 (Ang2), junctional adhesion molecule 2 (Jam2), bone morphogenic receptor type II (Bmpr2), and bone morphogenic protein 4 (Bmp4) were confirmed by quantitative PCR and/or immunoblotting using both primary cells and immortalized cells. Of these genes, our data suggest that Jam2, Bmpr2, and Bmp4 may be shear-sensitive in a p47phox-dependent manner. Taken together, our studies have identified a set of shear- and p47phox-sensitive genes, including unexpected and novel targets, which may play critical roles in vascular cell biology and pathobiology.

Atherosclerosis is a major cause of mortality in industrialized nations. Atherosclerosis is characterized by plaque deposition which decreases the lumen diameter into a stenosis. The creation of a restriction increases shear rates pathologic levels exceeding 3,500/s. Following plaque cap rupture, thrombus may form from the accumulation of millions of platelets, occluding the vessel, leading to heart attack and stroke. Studies of high shear thrombosis show that platelet activation, GPIIb/IIIa and vWF are involved. However, some recent studies also suggest that high shear aggregation is not dependent on activation or GPIIb/IIIa. Several antiplatelet pharmaceuticals against activation and GPIIb/IIIa have been proposed, but their efficacy in patients remains mixed. The overall objective of this project is to determine the factors necessary for thrombosis to occlusion in very high shear regions seen in diseased arteries. Our central hypotheses are that platelet activation and the subsequent conformational change in GPIIb/IIIa are necessary for thrombosis, and that higher concentrations of vWF in the plasma will increase thrombosis. To this end, we developed a new high shear hemodynamic model utilizing 30mLs of whole blood and quantified thrombus thickness, volume accumulation and accumulation rates. We demonstrate that thrombosis to occlusion stems from a second phase of Rapid Platelet Accumulation (RPA). Thrombus accumulation is completely prevented by PGE1 inhibition of platelet activation. Similarly, GPIIb/IIIa blockade via abciximab prevented significant thrombus deposition and RPA. We also found that increasing plasma vWF levels in high shear regions increased thrombus thickness and suggestively increased RPA rates. The results clarify the need for activation of mural platelets for long term thrombus accumulation without the activation of circulating platelets.

The development and testing of a shear cell for the purpose of measuring swash zone bed shear stress is presented. Direct measurements of bed shear stress were subsequently obtained using the shear plate in small, medium, and large-scale laboratory facilities. Measurements from both dam- break and bore-driven swash experiments are considered, covering a wide range of hydrodynamics and bed roughness. The dam-break problem is of interest here due to the theoretical analogy with the run-up of a solitary bore on a beach. Estimates of the flow velocities through the full swash cycle were obtained through numerical modelling and verified against measured velocity data. In conjunction, these data are used to calculate skin friction coefficients. The measurements indicate strong temporal and spatial variation in bed shear stress throughout the swash cycle, and a clear distinction between the uprush and backwash phase. For a single swash event, the maximum uprush bed shear stresses occur in the lower swash zone, within the range 0<x/Rx<0.3. The maximum backwash bed shear stresses also occur in the lower swash zone, and extend seaward of the initial bore collapse location. For a given cross-shore location the peak uprush bed shear stress is typically greater than the peak backwash bed shear stress by at least a factor two and up to a factor four. Local skin friction coefficients also indicate strong temporal and spatial variation. Furthermore, the behaviour of the local skin friction coefficient (back calculated from the measured bed shear stress using predicted, depth-averaged, flow velocities) over the swash cycle is inconsistent with the classical behaviour that is expected on the basis of the low Reynolds number flow. Smooth bed dam break and swash uprush friction coefficients appear to follow the general behaviour observed for smooth, turbulent open channel flow for an increasing Reynolds number. However, for a decreasing Reynolds number the behaviour of Cf differs from the steady flow relation. This is attributed the unsteady swash flow regime and flow history effects. It is expected that differences in flow history between the uprush and backwash have implications in terms of swash boundary layer growth and the resulting bed shear stress. A Lagrangian model for the swash boundary layer development is presented to consider these flow history effects. The model is based on the momentum integral approach for steady, turbulent, flat-plate boundary layers, with appropriate modifications to account for the unsteady flow regime. Fluid particle trajectories and velocity are computed and the boundary layer growth across the entire swash zone is estimated. Predictions of the bed shear stress agree well with the direct bed shear stress measurements and show a bias toward uprush sediment transport which has consistently been observed in measurements.