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

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

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

Allele specific repair of splicing mutations in cystic fibrosis through AsCas12a genome editing.

Funder: Fondazione Fibrosi Cistica - FFC#1/2017Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the CFTR gene. The 3272-26A>G and 3849+10kbC>T CFTR mutations alter the correct splicing of the CFTR gene, generating new acceptor and donor splice sites respectively. Here we develop a genome editing approach to permanently correct these genetic defects, using a single crRNA and the Acidaminococcus sp. BV3L6, AsCas12a. This genetic repair strategy is highly precise, showing very strong discrimination between the wild-type and mutant sequence and a complete absence of detectable off-targets. The efficacy of this gene correction strategy is verified in intestinal organoids and airway epithelial cells derived from CF patients carrying the 3272-26A>G or 3849+10kbC>T mutations, showing efficient repair and complete functional recovery of the CFTR channel. These results demonstrate that allele-specific genome editing with AsCas12a can correct aberrant CFTR splicing mutations, paving the way for a permanent splicing correction in genetic diseases