| 1. |
- Milanovic, J. V., et al.
(författare)
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International Industry Practice on Power Quality Monitoring
- 2014
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Ingår i: IEEE Transactions on Power Delivery. - 0885-8977 .- 1937-4208. ; 29:2, s. 934-941
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Tidskriftsartikel (refereegranskat)abstract
- Monitoring of voltages and currents at system buses gives the network operators information about the performance of their network, both for the system as a whole and for individual locations and customers. There is also demand from the customers and the regulatory agencies to provide information on the actual power-quality (PQ) level. Developments in enabling technology have made it possible to monitor at a large scale and to record virtually any PQ parameter of interest. While many network operators are installing monitoring equipment and while more and more monitors are available, there is a lack of knowledge and agreement on a number of aspects of the monitoring process and on processing the recorded data. As a response to this lack of uniformity in approach, data acquisition, and processing, in February 2011, CIGRE and CIRED established the Joint Working Group C4.112: “Guidelines for Power quality monitoring—measurement locations, processing and presentation of data.” In order to identify the current international industry practice on PQ monitoring, the group carried out a survey in 43 countries across the world. This paper summarizes the key findings from 114 responses to the questionnaire and identifies prevalent industrial practice in PQ monitoring around the world.
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| 2. |
- Padayachee, Eden R., 1986, et al.
(författare)
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Cerebrospinal fluid-induced retardation of amyloid beta aggregation correlates with Alzheimer's disease and the APOE epsilon 4 allele
- 2016
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Ingår i: Brain Research. - : Elsevier BV. - 0006-8993. ; 1651, s. 11-16
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Tidskriftsartikel (refereegranskat)abstract
- Misfolding and aggregation of amyloid beta (A beta) are key features of Alzheimer's disease (AD) pathogenesis, but the molecular events controlling this process are not known in detail. In vivo, A beta aggregation and plaque formation occur in the interstitial fluid of the brain extracellular matrix. This fluid communicates freely with cerebrospinal fluid (CSF). Here, we examined the effect of human CSF on A beta aggregation kinetics in relation to AD diagnosis and carrier status of the apolipoprotein E (APOE) epsilon 4 allele, the main genetic risk factor for sporadic AD. The aggregation of A beta was inhibited in the presence of CSF and, surprisingly, the effect was more pronounced in APOE epsilon 4 carriers. However, by fractionation of CSF using size exclusion chromatography, it became evident that it was not the ApoE protein itself that conveyed the inhibition, since the retarding species eluted at lower volume, corresponding to a much higher molecular weight, than ApoE monomers. Cholesterol quantification and immunoblotting identified high-density lipoprotein particles in the retarding fractions, indicating that such particles may be responsible for the inhibition. These results add information to the yet unresolved puzzle on how the risk factor of APOE epsilon 4 functions in AD pathogenesis. (C) 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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| 3. |
- Padayachee, E. R., et al.
(författare)
-
Cerebrospinal fluid-induced retardation of amyloid β aggregation correlates with Alzheimer's disease and the APOE ε4 allele
- 2016
-
Ingår i: Brain Research. - : Elsevier BV. - 0006-8993. ; 1651, s. 11-16
-
Tidskriftsartikel (refereegranskat)abstract
- Misfolding and aggregation of amyloid β (Aβ) are key features of Alzheimer's disease (AD) pathogenesis, but the molecular events controlling this process are not known in detail. In vivo, Aβ aggregation and plaque formation occur in the interstitial fluid of the brain extracellular matrix. This fluid communicates freely with cerebrospinal fluid (CSF). Here, we examined the effect of human CSF on Aβ aggregation kinetics in relation to AD diagnosis and carrier status of the apolipoprotein E (APOE) ε4 allele, the main genetic risk factor for sporadic AD. The aggregation of Aβ was inhibited in the presence of CSF and, surprisingly, the effect was more pronounced in APOE ε4 carriers. However, by fractionation of CSF using size exclusion chromatography, it became evident that it was not the ApoE protein itself that conveyed the inhibition, since the retarding species eluted at lower volume, corresponding to a much higher molecular weight, than ApoE monomers. Cholesterol quantification and immunoblotting identified high-density lipoprotein particles in the retarding fractions, indicating that such particles may be responsible for the inhibition. These results add information to the yet unresolved puzzle on how the risk factor of APOE ε4 functions in AD pathogenesis.
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