Optimal Sizing and Placing of Distributed Generation in Distribution Networks

Master of ScienceDepartment of Electrical and Computer EngineeringAnil PahwaDue to the ongoing changes in the structure of the electricity markets, distribution networks have developed an appealing potential for housing distributed generation (DG). In order to make the most out of the present distribution network, this project report verifies the results and method developed in a paper (Optimal Allocation of Embedded Generation on Distribution Networks) by A. Kean and M. O’Malley, which discusses an efficient way of incorporating DG in the current power system. The methodology under consideration elaborates on how certain constraints should be adopted that will lead toward optimally sizing and placing DG in the network under examination. Along with that, the effect of voltage rise and short circuit current are observed which shows that a certain allocation to some buses will cause a sudden rise in voltage and short circuit levels throughout the network. Furthermore, the adopted methodology with its relative constraints is solved using linear programming. Linear programming provides a more accurate allocation than its heuristic counterparts when it comes to embedding DG in smaller networks. The adopted methodology is then applied to a section of the Irish rural distribution network and the results pinpoint that appropriate placement of the DG will pave the way toward higher levels of penetration. The results obtained showed the same pattern as those recorded in the aforementioned source paper, there were only minor differences that are the result of using different software’s than those that were used by the authors of the paper

A Day Ahead Market Energy Auction for Distribution System Operation

In this paper, we study a day ahead double energy auction in a distribution system involving dispatchable generation units, renewable generation units supported by battery storage systems(BSSs), fixed loads, price responsive loads, and supply from the Whole Sale Market(WSM) at Locational Marginal Price(LMP). The auction is implemented within a Distribution System Operator (DSO) premises using Mixed Integer Linear Programming (MIP). The proposed auction is cleared at the Distribution LMP (DLMP) and is observed to be weakly budget balanced if no penalty is applied for DSO's deviation from originally committed supply from the WSM. Furthermore, the dynamics of LMP and DLMP, and their effect on distribution market participants scheduled quantities as well as the WSM supply to the distribution system is investigated.Comment: Electro Information Technology (EIT), 2017 IEEE International Conference o

Combined changes in Wnt signalling response and contact inhibition induce altered proliferation in radiation treated intestinal crypts

Curative intervention is possible if colorectal cancer is identified early, underscoring the need to detect the earliest stages of malignant transformation. A candidate biomarker is the expanded proliferative zone observed in crypts before adenoma formation, also found in irradiated crypts. However, the underlying driving mechanism for this is not known. Wnt signaling is a key regulator of proliferation, and elevated Wnt signaling is implicated in cancer. Nonetheless, how cells differentiate Wnt signals of varying strengths is not understood. We use computational modeling to compare alternative hypotheses about how Wnt signaling and contact inhibition affect proliferation. Direct comparison of simulations with published experimental data revealed that the model that best reproduces proliferation patterns in normal crypts stipulates that proliferative fate and cell cycle duration are set by the Wnt stimulus experienced at birth. The model also showed that the broadened proliferation zone induced by tumorigenic radiation can be attributed to cells responding to lower Wnt concentrations and dividing at smaller volumes. Application of the model to data from irradiated crypts after an extended recovery period permitted deductions about the extent of the initial insult. Application of computational modeling to experimental data revealed how mechanisms that control cell dynamics are altered at the earliest stages of carcinogenesis

2D versus 3D human induced pluripotent stem cell-derived cultures for neurodegenerative disease modelling

Neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and amyotrophic lateral sclerosis (ALS), affect millions of people every year and so far, there are no therapeutic cures available. Even though animal and histological models have been of great aid in understanding disease mechanisms and identifying possible therapeutic strategies, in order to find disease-modifying solutions there is still a critical need for systems that can provide more predictive and physiologically relevant results. One possible avenue is the development of patient-derived models, e.g. by reprogramming patient somatic cells into human induced pluripotent stem cells (hiPSCs), which can then be differentiated into any cell type for modelling. These systems contain key genetic information from the donors, and therefore have enormous potential as tools in the investigation of pathological mechanisms underlying disease phenotype, and progression, as well as in drug testing platforms. hiPSCs have been widely cultured in 2D systems, but in order to mimic human brain complexity, 3D models have been proposed as a more advanced alternative. This review will focus on the use of patient-derived hiPSCs to model AD, PD, HD and ALS. In brief, we will cover the available stem cells, types of 2D and 3D culture systems, existing models for neurodegenerative diseases, obstacles to model these diseases in vitro, and current perspectives in the field

Paneth cell - rich regions separated by a cluster of Lgr5+ cells initiate crypt fission in the intestinal stem cell niche

The crypts of the intestinal epithelium house the stem cells that ensure the continual renewal of the epithelial cells that line the intestinal tract. Crypt number increases by a process called crypt fission, the division of a single crypt into two daughter crypts. Fission drives normal tissue growth and maintenance. Correspondingly, it becomes less frequent in adulthood. Importantly, fission is reactivated to drive adenoma growth. The mechanisms governing fission are poorly understood. However, only by knowing how normal fission operates can cancer-associated changes be elucidated. We studied normal fission in tissue in three dimensions using high-resolution imaging and used intestinal organoids to identify underlying mechanisms. We discovered that both the number and relative position of Paneth cells and Lgr5+ cells are important for fission. Furthermore, the higher stiffness and increased adhesion of Paneth cells are involved in determining the site of fission. Formation of a cluster of Lgr5+ cells between at least two Paneth-cell-rich domains establishes the site for the upward invagination that initiates fission

Interkinetic nuclear migration and basal tethering facilitates post-mitotic daughter separation in intestinal organoids

Homeostasis of renewing tissues requires balanced proliferation, differentiation and movement. This is particullary important in the intestinal epithelium where lineage tracing suggests that stochastic differentiation choices are intricately coupled to position relative to a niche. To determine how position is achieved we followed proliferating cells in intestinal organoids and discovered that behaviour of mitotic sisters predicted long-term positioning. We found that normally, 70% of sisters remain neighbours while 30% lose contact and separate after cytokinesis. These post-mitotic placements predict longer term differences in positions assumed by sisters: adjacent sisters reach similar positions over time; in a pair of separating sisters, one remains close to its birthplace while the other is displaced upward. Computationally modelling crypt dynamics confirmed that post-mitotic separation leads to sisters reaching different compartments. We show that interkinetic nuclear migration, cell size, and asymmetric tethering by a basal process contribute to separations. These processes are altered in Adenomatous polyposis coli (Apc) mutant epithelia where separation is lost. We conclude that post-mitotic placement contributes to stochastic niche exit and when defective, supports the clonal expansion of Apc mutant cells

Interactions of the 67 kDa laminin receptor and its precursor with laminin

The 67LR (67 kDa laminin receptor) enables cells to interact with components of the extracellular matrix. The molecule is derived from the 37LRP (37 kDa laminin receptor precursor); however, the precise molecular mechanism of this conversion is unknown. Recombinant 37LRP, expressed in and purified from Escherichia coli, bound to human laminin in a SPR (surface plasmon resonance) experiment. 67LR isolated from human breast-cancer-derived cells in culture was also shown to bind to laminin by SPR. However, the kinetics of association are qualitatively different. 37LRP, but not 67LR, binds to heparan sulfate. The binding of 37LRP to heparan sulfate did not affect the interaction of 37LRP with laminin. In contrast, heparan sulfate reduces the extent of binding of laminin to 67LR. Taken together, these results show that 37LRP has some of the biological activities of 67LR, even prior to the conversion event. However, the conversion affects the sites of interaction with both laminin and heparan sulfate