A CFD analysis of the pollutant dispersion from cooling towers with various configurations in the lower region of atmospheric boundary layer.

The mixing and merging of buoyant plumes originating from multiple small cooling towers into the atmosphere is numerically investigated. The effects of different arrangements of cooling towers as well as outlet geometries on the mixing of the plumes are examined. The side by side and tandem arrangements of two sources and also two types of multi-flue cooling towers are considered. The various ways by which the counter rotating vortex pair, as the dominant mechanism, affect the flow pattern in each aforementioned configuration are investigated. For tandem arrangement, far from sources, the outlet flow of the downstream cooling tower surrounds the plumes originating from the upstream cooling tower and in the region near the cooling towers, the pollutants are mostly originated from the upstream cooling tower. Maximum pollutant concentrations at distances 10 and 40 times the diameter downstream of the leading cooling tower increase by 67% and 29% with respect to those of a single cooling tower, respectively. For the side by side arrangement, the counter rotating vortices are stretched due to the large low pressure area created downstream of the cooling towers. Mixing of the plumes with the surrounding air is reduced as a result of contraction of vortices. Maximum contaminant concentrations at distances 10 and 40 times the diameter downstream of the cooling towers increase by 29% and 41% with respect to those of a single tower, respectively. Finally, the differences between flow fields formed around diamond and square configurations of multi-flue cooling towers are extensively discussed.

Correction: The Vital Role of Blood Flow-Induced Proliferation and Migration in Capillary Network Formation in a Multiscale Model of Angiogenesis.

[This corrects the article DOI: 10.1371/journal.pone.0128878.].

Blood flow and endothelial cell phenotype regulation during sprouting angiogenesis.

The role of the endothelial cell environment and shear stress induced by blood flow in phenotype determination and lumen formation has been clearly illustrated in recent studies. In the present work, a model is developed to map environmental and flow induced signals in sprouting angiogenesis to endothelial cell phenotype and lumen formation. To follow the endothelial cell lumen formation, its signaling pathway is incorporated in the present work within the phenotype determination pathway that has been recently utilized to model endothelial cell migration, proliferation, and apoptosis. Moreover, a signaling cascade for shear stress activation of endothelial cells is proposed and used for phenotype determination with activation of blood flow. A Boolean network model is employed to build a hybrid map for the relation between the endothelial cell environmental signals and the endothelial cell fate in sprouting angiogenesis with and without blood flow. This map is very useful in the development of models for sprouting angiogenesis. Moreover, this study shows that inhibition of intracellular signaling molecules, solely or in pairs, blocks angiogenic-signaling pathways and can be used to inhibit angiogenesis.

Activation of Apoptotic Signal in Endothelial Cells through Intracellular Signaling Molecules Blockade in Tumor-Induced Angiogenesis.

Tumor-induced angiogenesis is the bridge between avascular and vascular tumor growth phases. In tumor-induced angiogenesis, endothelial cells start to migrate and proliferate toward the tumor and build new capillaries toward the tumor. There are two stages for sprout extension during angiogenesis. The first stage is prior to anastomosis, when single sprouts extend. The second stage is after anastomosis when closed flow pathways or loops are formed and blood flows in the closed loops. Prior to anastomosis, biochemical and biomechanical signals from extracellular matrix regulate endothelial cell phenotype; however, after anastomosis, blood flow is the main regulator of endothelial cell phenotype. In this study, the critical signaling pathways of each stage are introduced. A Boolean network model is used to map environmental and flow induced signals to endothelial cell phenotype (proliferation, migration, apoptosis, and lumen formation). Using the Boolean network model, blockade of intracellular signaling molecules of endothelial cell is investigated prior to and after anastomosis and the cell fate is obtained in each case. Activation of apoptotic signal in endothelial cell can prevent the extension of new vessels and may inhibit angiogenesis. It is shown that blockade of a few signaling molecules in endothelial cell activates apoptotic signal that are proposed as antiangiogenic strategies.

The Vital Role of Blood Flow-Induced Proliferation and Migration in Capillary Network Formation in a Multiscale Model of Angiogenesis.

Sprouting angiogenesis and capillary network formation are tissue scale phenomena. There are also sub-scale phenomena involved in angiogenesis including at the cellular and intracellular (molecular) scales. In this work, a multiscale model of angiogenesis spanning intracellular, cellular, and tissue scales is developed in detail. The key events that are considered at the tissue scale are formation of closed flow path (that is called loop in this article) and blood flow initiation in the loop. At the cellular scale, growth, migration, and anastomosis of endothelial cells (ECs) are important. At the intracellular scale, cell phenotype determination as well as alteration due to blood flow is included, having pivotal roles in the model. The main feature of the model is to obtain the physical behavior of a closed loop at the tissue scale, relying on the events at the cellular and intracellular scales, and not by imposing physical behavior upon it. Results show that, when blood flow is considered in the loop, the anastomosed sprouts stabilize and elongate. By contrast, when the loop is modeled without consideration of blood flow, the loop collapses. The results obtained in this work show that proper determination of EC phenotype is the key for its survival.

Effect of tumor shape, size, and tissue transport properties on drug delivery to solid tumors.

BACKGROUND: The computational methods provide condition for investigation related to the process of drug delivery, such as convection and diffusion of drug in extracellular matrices, drug extravasation from microvessels or to lymphatic vessels. The information of this process clarifies the mechanisms of drug delivery from the injection site to absorption by a solid tumor. In this study, an advanced numerical method is used to solve fluid flow and solute transport equations simultaneously to investigate the effect of tumor shape and size on drug delivery to solid tumor. METHODS: The advanced mathematical model used in our previous work is further developed by adding solute transport equation to the governing equations. After applying appropriate boundary and initial conditions on tumor and surrounding tissue geometry, the element-based finite volume method is used for solving governing equations of drug delivery in solid tumor. Also, the effects of size and shape of tumor and some of tissue transport parameters such as effective pressure and hydraulic conductivity on interstitial fluid flow and drug delivery are investigated. RESULTS: Sensitivity analysis shows that drug delivery in prolate shape is significantly better than other tumor shapes. Considering size effect, increasing tumor size decreases drug concentration in interstitial fluid. This study shows that dependency of drug concentration in interstitial fluid to osmotic and intravascular pressure is negligible. CONCLUSIONS: This study shows that among diffusion and convection mechanisms of drug transport, diffusion is dominant in most different tumor shapes and sizes. In tumors in which the convection has considerable effect, the drug concentration is larger than that of other tumors at the same time post injection.