Reliability and Cost Model of P.M. in A Component of an Electrical Distribution System Considering Ageing Mechanism

Application of Reliability Centered Maintenance (RCM) in a system results in a decrease in component failure rates and as such improvement in the system reliability. One of the major subjects of the RCM is focused on the Online and Offline Preventive Maintenance (OPM and FPM which together will be denoted by OFPM) of the components which repairing the component needs or doesn’t need to stop the mission carrying out by it. The RCM is classified as a preventive maintenance policy and has significant contribution in practical applications. However, little research has been devoted to modeling the online and offline Preventive Maintenance. This research assumes that the component failure rate will be improved if the OFPM is performed for a long period of time as a part of an RCM program. Application of an OFPM program could cause the component set at least to “as bad as old state but cannot reach the “as good as new” state. The emphasis of this research is to model the OFPM for critical components or any equipment with critical failure in a system. The proposed model is based on the concept of PM and improvement factor of reliability in a system with critical components which their failure could cause a failure in the system (first-order cut- sets).DOI:http://dx.doi.org/10.11591/ijece.v4i2.551

Customer choice of reliability in spinning reserve procurement and cost allocation using well-being analysis,” Elect

a b s t r a c t A novel pool-based market-clearing algorithm for spinning reserve (SR) procurement and the cost allocation associated with provision of spinning reserve among customers (DisCos) is developed in this paper. Rational buyer market model is used to clear energy and spinning reserve markets in the proposed algorithm. This market model gives DisCos the opportunity to declare their own energy requirement together with their desired reliability levels to the ISO and also they can participate in the SR market as a interruptible load. The DisCos' desired reliability levels are selected from a hybrid deterministic/probabilistic framework designated as the system well-being model. Using the demand of each DisCo and its associated desired reliability level, the overall desired system reliability level is determined. The market operator then purchases spinning reserve commodity from the associated market such that the overall desired system reliability level is satisfied. A methodology is developed in this paper to fairly allocate the cost associated with providing spinning reserve among DisCos based on their demands and desired reliability levels. An algorithm is also presented in this paper for implementing the proposed approach. The effectiveness of the proposed technique is examined using the IEEE-RTS

Editorial: Climate change mitigation and adaptation in power and energy systems

\ua9 2024. This editorial summarizes the papers selected for publication in the Special Issue on Climate Change Mitigation and Adaptation in Power and Energy Systems (CMAP). After a rigorous review of 86 submitted manuscripts, 23 papers were accepted for publication. These accepted papers cover various aspects of climate change mitigation and adaptation and are classified as follows: boosting renewable energy efficiency (two papers), climate resilience strategies (four papers), decarbonization strategies (four papers), renewable energy integration (five papers), policies, incentives, and science communications (four papers), and the role of energy markets (four papers). The Guest Editorial Board is optimistic that this Special Issue will serve as a rich resource, offering invaluable insights to propel future research and advancements in climate change mitigation and adaptation

SIRT3 Mediates Multi-Tissue Coupling for Metabolic Fuel Switching

SummarySIRT3 is a member of the Sirtuin family of NAD+-dependent deacylases and plays a critical role in metabolic regulation. Organism-wide SIRT3 loss manifests in metabolic alterations; however, the coordinating role of SIRT3 among metabolically distinct tissues is unknown. Using multi-tissue quantitative proteomics comparing fasted wild-type mice to mice lacking SIRT3, innovative bioinformatic analysis, and biochemical validation, we provide a comprehensive view of mitochondrial acetylation and SIRT3 function. We find SIRT3 regulates the acetyl-proteome in core mitochondrial processes common to brain, heart, kidney, liver, and skeletal muscle, but differentially regulates metabolic pathways in fuel-producing and fuel-utilizing tissues. We propose an additional maintenance function for SIRT3 in liver and kidney where SIRT3 expression is elevated to reduce the acetate load on mitochondrial proteins. We provide evidence that SIRT3 impacts ketone body utilization in the brain and reveal a pivotal role for SIRT3 in the coordination between tissues required for metabolic homeostasis

A population-based dataset concerning predictors of willingness to get a COVID-19 vaccine in Iran

The global issue of preventing the spread of COVID-19 is challenging. One of the most efficient ways to control the pandemic is to have a full coverage of COVID-19 vaccination. Therefore, this paper collected survey data to understand the intention and willingness of COVID-19 vaccination uptake in Qazvin, Iran. With the use of a paper-and-pencil method and multistage stratified cluster sampling, research personnel approached and interviewed a representative sample of adults in Qazvin (n = 10843) between February 19 and April 9, 2021. The survey asked questions regarding sociodemographic information, fear of COVID-19, perceived COVID-19 infectability, perceived behavioral control over COVID-19 vaccination, subjective norm of COVID-19 vaccination, attitude towards COVID-19 vaccination, and intention to get COVID-19 vaccinated. The data collected from this survey were analyzed using descriptive statistics, which were carried out using the IBM SPSS version 17.0

Hippocampus size does not correlate with body mass index in bipolar disorder

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Kidney Pathology Precedes and Predicts the Pathological Cascade of Cerebrovascular Lesions in Stroke Prone Rats

INTRODUCTION: Human cerebral small vessel disease (CSVD) has been hypothesized to be an age-dependent disease accompanied by similar vascular changes in other organs. SHRSP feature numerous vascular risk factors and may be a valid model of some aspects of human CSVD. Here we compare renal histopathological changes with the brain pathology of spontaneously hypertensive stroke-prone rats (SHRSP). MATERIAL AND METHODS: We histologically investigated the brains and kidneys of 61 SHRSP at different stages of age (12 to 44 weeks). The brain pathology (aggregated erythrocytes in capillaries and arterioles, microbleeds, microthromboses) and the kidney pathology (aggregated erythrocytes within peritubular capillaries, tubular protein cylinders, glomerulosclerosis) were quantified separately. The prediction of the brain pathology by the kidney pathology was assessed by creating ROC-curves integrating the degree of kidney pathology and age of SHRSP. RESULTS: Both, brain and kidney pathology, show an age-dependency and proceed in definite stages whereas an aggregation of erythrocytes in capillaries and arterioles, we parsimoniously interpreted as stases, represent the initial finding in both organs. Thus, early renal tubulointerstitial damage characterized by rather few intravasal erythrocyte aggregations and tubular protein cylinders predicts the initial step of SHRSPs' cerebral vascular pathology marked by accumulated erythrocytes. The combined increase of intravasal erythrocyte aggregations and protein cylinders accompanied by glomerulosclerosis and thrombotic renal microangiopathy in kidneys of older SHRSP predicts the final stages of SHRSPs' cerebrovascular lesions marked by microbleeds and thrombotic infarcts. CONCLUSION: Our results illustrate a close association between structural brain and kidney pathology and support the concept of small vessel disease to be an age-dependent systemic pathology. Further, an improved joined nephrologic and neurologic diagnostic may help to identify patients with CSVD at an early stage

Metabotyping of docosahexaenoic acid - Treated alzheimer's disease cell model

10.1371/journal.pone.0090123PLoS ONE92-POLN

Diacylglycerol kinase β promotes dendritic outgrowth and spine maturation in developing hippocampal neurons

<p>Abstract</p> <p>Background</p> <p>Diacylglycerol kinase (DGK) is an enzyme that phosphorylates diacylglycerol to phosphatidic acid and comprises multiple isozymes of distinct properties. Of DGKs, mRNA signal for DGKβ is strongly detected in the striatum, and one of the transcripts derived from the human DGKβ locus is annotated in GenBank as being differentially expressed in bipolar disorder patients. Recently, we have reported that DGKβ is expressed in medium spiny neurons of the striatum and is highly concentrated at the perisynapse of dendritic spines. However, it remains elusive how DGKβ is implicated in pathophysiological role in neurons at the cellular level.</p> <p>Results</p> <p>In the present study, we investigated the expression and subcellular localization of DGKβ in the hippocampus, together with its functional implication using transfected hippocampal neurons. DGKβ is expressed not only in projection neurons but also in interneurons and is concentrated at perisynaptic sites of asymmetrical synapses. Overexpression of wild-type DGKβ promotes dendrite outgrowth at 7 d in <it>vitro </it>(DIV) and spine maturation at 14 DIV in transfected hippocampal neurons, although its kinase-dead mutant has no effect.</p> <p>Conclusion</p> <p>In the hippocampus, DGKβ is expressed in both projection neurons and interneurons and is accumulated at the perisynapse of dendritic spines in asymmetrical synapses. Transfection experiments suggest that DGKβ may be involved in the molecular machineries of dendrite outgrowth and spinogenesis through its kinase activity.</p

Docosahexaenoic Acid-Derived Neuroprotectin D1 Induces Neuronal Survival via Secretase- and PPARγ-Mediated Mechanisms in Alzheimer's Disease Models

Neuroprotectin D1 (NPD1) is a stereoselective mediator derived from the omega-3 essential fatty acid docosahexaenoic acid (DHA) with potent inflammatory resolving and neuroprotective bioactivity. NPD1 reduces Aβ42 peptide release from aging human brain cells and is severely depleted in Alzheimer's disease (AD) brain. Here we further characterize the mechanism of NPD1's neurogenic actions using 3xTg-AD mouse models and human neuronal-glial (HNG) cells in primary culture, either challenged with Aβ42 oligomeric peptide, or transfected with beta amyloid precursor protein (βAPP)sw (Swedish double mutation APP695sw, K595N-M596L). We also show that NPD1 downregulates Aβ42-triggered expression of the pro-inflammatory enzyme cyclooxygenase-2 (COX-2) and of B-94 (a TNF-α-inducible pro-inflammatory element) and apoptosis in HNG cells. Moreover, NPD1 suppresses Aβ42 peptide shedding by down-regulating β-secretase-1 (BACE1) while activating the α-secretase ADAM10 and up-regulating sAPPα, thus shifting the cleavage of βAPP holoenzyme from an amyloidogenic into the non-amyloidogenic pathway. Use of the thiazolidinedione peroxisome proliferator-activated receptor gamma (PPARγ) agonist rosiglitazone, the irreversible PPARγ antagonist GW9662, and overexpressing PPARγ suggests that the NPD1-mediated down-regulation of BACE1 and Aβ42 peptide release is PPARγ-dependent. In conclusion, NPD1 bioactivity potently down regulates inflammatory signaling, amyloidogenic APP cleavage and apoptosis, underscoring the potential of this lipid mediator to rescue human brain cells in early stages of neurodegenerations