208 resultados para Loss allocation

em QUB Research Portal - Research Directory and Institutional Repository for Queen's University Belfast


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This paper presents a new method for transmission loss allocation. The method is based on tracing the complex power flow through the network and determining the share of each load on the flow and losses through each line. Transmission losses are taken into consideration during power flow tracing. Unbundling line losses is carried out using an equation, which has a physical basis, and considers the coupling between active and reactive power flows as well as the cross effects of active and reactive power on active and reactive losses. A tracing algorithm which can be considered direct to a good extent, as there is no need for exhaustive search to determine the flow paths as these are determined in a systematic way during the course of tracing. Results of application of the proposed method are also presented.

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This paper presents a new method for transmission loss allocation in a deregulated electrical power market. The proposed method is based on physical flow through transmission lines. The contributions of individual loads to the line flows are used as basis for allocating transmission losses to different loads. With minimum assumptions, that sound to be reasonable and cannot be rejected, a novel loss allocation formula is derived. The assumptions made are: a number of currents sharing a transmission line distribute themselves over the cross section in the same manner; that distribution causes the minimum possible power loss. Application of the proposed method is straightforward. It requires only a solved power flow and any simple algorithm for power flow tracing. Both active and reactive powers are considered in the loss allocation procedure. Results of application show the accuracy of the proposed method compared with the commonly used procedures.

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A new method is presented for transmission loss allocation based on the separation of transmission loss caused by load and the loss due to circulating currents between generators. The theoretical basis for and derivation of the loss formulae are presented using simple systems. The concept is then extended to a general power system using the Ybus model. Details of the application of the proposed method to a typical power system are presented along with results from the IEEE 30 bus test system. The results from both the small system and the standard IEEE test system demonstrate the validity of the proposed method.

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This study presents a new method for determining the transmission network usage by loads and generators, which can then be used for transmission cost/loss allocation in an explainable and justifiable manner. The proposed method is based on solid physical grounds and circuit theory. It relies on dividing the currents through the network into two components; the first one is attributed to power flows from generators to loads, whereas the second one is because of the generators only. Unlike almost all the available methods, the proposed method is assumption free and hence it is more accurate than similar methods even those having some physical basis. The proposed method is validated through a transformer analogy, and theoretical derivations. The method is verified through application to the IEEE 30 bus system and the IEEE 118 test system. The results obtained verified many desirable features of the proposed method. Being more accurate in determining the network usage, in an explainable transparent manner, and in giving accurate cost signals, indicating the best locations to add loads and generation, are among the many desirable features.

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Studies suggest that activation of phosphoinositide 3-kinase-Akt may protect against neuronal cell death in Alzheimer's disease (AD). Here, however, we provide evidence of increased Akt activation, and hyperphosphorylation of critical Akt substrates in AD brain, which link to AD pathogenesis, suggesting that treatments aiming to activate the pathway in AD need to be considered carefully. A different distribution of Akt and phospho-Akt was detected in AD temporal cortex neurons compared with control neurons, with increased levels of active phosphorylated-Akt in particulate fractions, and significant decreases in Akt levels in AD cytosolic fractions, causing increased activation of Akt (phosphorylated-Akt/total Akt ratio) in AD. In concordance, significant increases in the levels of phosphorylation of total Akt substrates, including: GSK3ßSer9, tauSer214, mTORSer2448, and decreased levels of the Akt target, p27kip1, were found in AD temporal cortex compared with controls. A significant loss and altered distribution of the major negative regulator of Akt, PTEN (phosphatase and tensin homologue deleted on chromosome 10), was also detected in AD neurons. Loss of phosphorylated-Akt and PTEN-containing neurons were found in hippocampal CA1 at end stages of AD. Taken together, these results support a potential role for aberrant control of Akt and PTEN signalling in AD.