904 research outputs found

    An Adaptive Overcurrent Coordination Scheme to Improve Relay Sensitivity and Overcome Drawbacks due to Distributed Generation in Smart Grids

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    Distributed Generation (DG) brought new challenges for protection engineers since standard relay settings of traditional system may no longer function properly under increasing presence of DG. The extreme case is coordination loss between primary and backup relays. The directional overcurrent relay (DOCR) which is the most implemented protective device in the electrical network also suffers performance degradation in presence of DG. Therefore, this paper proposes the mitigation of DG impact on DOCR coordination employing adaptive protection scheme (APS) using differential evolution algorithm (DE) while improving overall sensitivity of relays . The impacts of DG prior and after the application of APS are presented based on interconnected 6 bus and IEEE 14 bus system. As a consequence, general sensitivity improvement and mitigation scheme is proposed

    Real time coordination of overcurrent relays by means of optimization algorithm.

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    Protection is widely used in all different voltage levels of the electrical power system: generation, transmission, sub-transmission and distribution etc. An overcurrent relay is a protection that is widely implemented in the sub-transmission and distribution systems due to its competing cost. Depending on the operative conditions and fault locations in a mesh system, the load or fault currents can circle in or out of the overcurrent relay's protective zone. Hence directional overcurrent relays are used to discriminate whether the fault is located in or out of the protective zone. The propose of coordinating the overcurrent relays is to encounter settings that minimize the operation time for faults within the protective zone and at the same time offering pre-specified timed backup for relays that are in the adjacent zones. So the maximum fault current that the relay detects in its protective zone must be greater than the fault currents in the adjacent zones. The above condition is met in radial systems, one source mesh systems and two source mesh systems where the sources are located symmetrically at the end. But the above condition is not always met in the multi-source mesh systems due to the numerous operative configurations. Since the systems cannot operate in the absence of protection, other protection principles must be used, i.e. impedance relay. It is then said that for certain operative configurations of mesh system, overcurrent protection principle is out of range or in other words reaches the limit of its protection principle [1]

    Enterovirus type 71 2A protease functions as a transcriptional activator in yeast

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    Enterovirus type 71 (EV71) 2A protease exhibited strong transcriptional activity in yeast cells. The transcriptional activity of 2A protease was independent of its protease activity. EV71 2A protease retained its transcriptional activity after truncation of 40 amino acids at the N-terminus but lost this activity after truncation of 60 amino acids at the N-terminus or deletion of 20 amino acids at the C-terminus. Thus, the acidic domain at the C-terminus of this protein is essential for its transcriptional activity. Indeed, deletion of amino acids from 146 to 149 (EAME) in this acidic domain lost the transcriptional activity of EV71 2A protein though still retained its protease activity. EV71 2A protease was detected both in the cytoplasm and nucleus using confocal microscopy analysis. Coxsackie virus B3 2A protease also exhibited transcriptional activity in yeast cells. As expected, an acidic domain in the C-terminus of Coxsackie virus B3 2A protease was also identified. Truncation of this acidic domain resulted in the loss of transcriptional activity. Interestingly, this acidic region of poliovirus 2A protease is critical for viral RNA replication. The transcriptional activity of the EV71 or Coxsackie virus B3 2A protease should play a role in viral replication and/or pathogenesis

    Dysfunction of the noradrenergic system drives inflammation, α-synucleinopathy, and neuronal loss in mouse colon

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    Clinical and pathological evidence revealed that α-synuclein (α-syn) pathology seen in PD patients starts in the gut and spreads via anatomically connected structures from the gut to the brain. Our previous study demonstrated that depletion of central norepinephrine (NE) disrupted brain immune homeostasis, producing a spatiotemporal order of neurodegeneration in the mouse brain. The purpose of this study was 1) to determine the role of peripheral noradrenergic system in the maintenance of gut immune homeostasis and in the pathogenesis of PD and 2) to investigate whether NE-depletion induced PD-like α-syn pathological changes starts from the gut. For these purposes, we investigated time-dependent changes of α-synucleinopathy and neuronal loss in the gut following a single injection of DSP-4 (a selective noradrenergic neurotoxin) to A53T-SNCA (human mutant α-syn) over-expression mice. We found DPS-4 significantly reduced the tissue level of NE and increased immune activities in gut, characterized by increased number of phagocytes and proinflammatory gene expression. Furthermore, a rapid-onset of α-syn pathology was observed in enteric neurons after 2 weeks and delayed dopaminergic neurodegeneration in the substantia nigra was detected after 3-5 months, associated with the appearance of constipation and impaired motor function, respectively. The increased α-syn pathology was only observed in large, but not in the small, intestine, which is similar to what was observed in PD patients. Mechanistic studies reveal that DSP-4-elicited upregulation of NADPH oxidase (NOX2) initially occurred only in immune cells during the acute intestinal inflammation stage, and then spread to enteric neurons and mucosal epithelial cells during the chronic inflammation stage. The upregulation of neuronal NOX2 correlated well with the extent of α-syn aggregation and subsequent enteric neuronal loss, suggesting that NOX2-generated reactive oxygen species play a key role in α-synucleinopathy. Moreover, inhibiting NOX2 by diphenyleneiodonium or restoring NE function by salmeterol (a β2-receptor agonist) significantly attenuated colon inflammation, α-syn aggregation/propagation, and enteric neurodegeneration in the colon and ameliorated subsequent behavioral deficits. Taken together, our model of PD shows a progressive pattern of pathological changes from the gut to the brain and suggests a potential role of the noradrenergic dysfunction in the pathogenesis of PD

    An Obesity Paradox of Asian Body Mass Index after Cardiac Surgery: Arterial Oxygenations in Duration of Mechanic Ventilation

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    Background. Numerous studies have documented an obesity paradox that overweight of Caucasian patients has better prognosis after cardiac surgery. This study is to examine Asian patients’ BMI to see whether an obesity paradox exists in DMV after cardiac surgery. Methods. A retrospective study consisted of 428 patients after cardiac surgery from January 2006 to December 2010 in the medical center of Taiwan. The Asian BMI was divided into 3 groups: under-normal weight patients (; ), overweight patients (BMI 24 to <27; ), and obese patients (; ). Multivariable analysis and paired were used to compare all variables. Results. Overweight patients were significantly associated with the shortest DMV. Under-normal weight patients had significantly better oxygenations of AaDO2 and P/F ratio in the DMV; however, they correlated with the longest DMV, older age, more female, lower LVSV, higher BUN, more dialysis-dependent, and poorer outcomes, namely, 1-year mortality, HAP, reintubation, tracheotomy, and LOS. Conclusions. Asian overweight patients after cardiac surgery have better prognosis. Under-normal weight patients have higher risk factors, longer DMV, and poorer outcomes; even though they have better arterial oxygenations, they seem to need better arterial oxygenations for successful weaning ventilator

    The Application of Borehole Hydrogeological Investigation for Assessing Landslide Susceptibility

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    On the basis of 49 borehole studies at the mid- and upper-stream of the Dajia and Jhuoshuei river basins, landslide occurrence was found to not only be related to subsurface geological composition and hydrogeological characteristics, but also to groundwater level dynamics, which have seldom been addressed in previous works. It is suggested that the interplay between hydrogeologic and landslide factors be given further consideration in future investigations. This would be a crucial step towards effective disaster prevention for mountainous regions in Taiwan.本研究主要係嘗試透過孔內水文地質調查結果,評估大甲溪與濁水溪流域地表下岩層的地質材料特性、水力特性、地下水與集水區山崩潛勢之關聯性。過去研究較少針對崩塌地進行現地水文地質調查與試驗,本研究根據49處試驗場址成果顯示,水文地質特性與山崩的潛勢、滑動深度,以及地下水位有一定程度之關聯性。本研究建議進行調查區域的水文地質特性,以及各促崩因子所造成的山崩的易損性,係各類型山崩災害分析與潛勢評估之重要的研究各題,亦可提供相關台灣災害防治之參考

    High levels of serum macrophage migration inhibitory factor and interleukin 10 are associated with a rapidly fatal outcome in patients with severe sepsis

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    SummaryObjectivesThe aim of this study was to delineate the association between high macrophage migration inhibitory factor (MIF) and interleukin 10 (IL-10) levels in the early phase of sepsis and rapidly fatal outcome.MethodsOne hundred and fifty-three adult subjects with the main diagnosis of severe sepsis (including septic shock) admitted directly from the emergency department of two tertiary medical centers and one regional teaching hospital between January 2009 and December 2011, were included prospectively. MIF and IL-10 levels were measured and outcomes were analyzed by Cox regression analysis according to the following outcomes: rapidly fatal outcome (RFO, death within 48h), late fatal outcome (LFO, death between 48h and 28 days), and survival at 28 days.ResultsAmong the three outcome groups, IL-10 levels were significantly higher in the RFO group (p < 0.001) and no significant differences were seen between the LFO and survivor groups. After Cox regression analysis, each incremental elevation of 1000 pg/ml in both IL-10 and MIF was independently associated with RFO in patients with severe sepsis. Each incremental elevation of 1000 pg/ml in IL-10 increased the RFO risk by a factor of 1.312 (95% confidence interval 1.094–1.575; p=0.003); this was the most significant factor leading to RFO in patients with severe sepsis.ConclusionsPatients with RFO exhibited simultaneously high MIF and IL-10 levels in the early phase of severe sepsis. Incremental increases in both IL-10 and MIF levels were associated with RFO in this patient group, and of the two, IL-10 was the most significant factor linked to RFO

    Anti-Nogo-A Immunotherapy Does Not Alter Hippocampal Neurogenesis after Stroke in Adult Rats

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    Ischemic stroke is a leading cause of adult disability, including cognitive impairment. Our laboratory has previously shown that treatment with function-blocking antibodies against the neurite growth inhibitory protein Nogo-A promotes functional recovery after stroke in adult and aged rats, including enhancing spatial memory performance, for which the hippocampus is critically important. Since spatial memory has been linked to hippocampal neurogenesis, we investigated whether anti-Nogo-A treatment increases hippocampal neurogenesis after stroke. Adult rats were subject to permanent middle cerebral artery occlusion followed 1 week later by 2 weeks of antibody treatment. Cellular proliferation in the dentate gyrus was quantified at the end of treatment, and the number of newborn neurons was determined at 8 weeks post-stroke. Treatment with both anti-Nogo-A and control antibodies stimulated the accumulation of new microglia/macrophages in the dentate granule cell layer, but neither treatment increased cellular proliferation or the number of newborn neurons above stroke-only levels. These results suggest that anti-Nogo-A immunotherapy does not increase post-stroke hippocampal neurogenesis
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