Distributed control strategy for DC microgrids based on average consensus and fractional-order local controllers

A novel distributed secondary layer control strategy based on average consensus and fractional-order proportional-integral (FOPI) local controllers is proposed for the regulation of the bus voltages and energy level balancing of the energy storage systems (ESSs) in DC microgrids. The distributed consensus protocol works based on an undirected sparse communication network. Fractional-order local controllers increase the degree of freedom in the tuning of closed-loop controllers, which is required for DC microgrids with high order dynamics. Therefore, here, FOPI local controllers are proposed for enhanced energy balancing of ESSs and improved regulation of the bus voltages across the microgrid. The proposed control strategy operates in both islanded and grid-connected modes of a DC microgrid. In both modes, the average voltage of the microgrid converges to the microgrid desired reference voltage. The charging/discharging of ESSs is controlled independent of the microgrid operating mode to maintain a balanced energy level. The performance of the proposed distributed control strategy is validated in a 38- V DC microgrid case study, simulated by Simulink real-time desktop, consisting of 10 buses and a photovoltaic renewable energy source

Functional characterisation of the methionine sulfoxide reductase repertoire in Trypanosoma brucei

We thank Guy Hanke (QMUL) for their critical review of this manuscript. We acknowledge the members of the T. brucei genome (http://tritrypdb.org/tritrypdb/) and TrypTag (http://tryptag.org) projects for sequence and localisation data, respectively. A component of this work was supported by grants from ANPCyT (PICT-2015-1149; PICT-2014-2103). SAG, and DGA are investigator career members from CONICET. AK was a recipient of a Queen Mary University of London PhD studentshi

Sexual Size Dimorphism and Body Condition in the Australasian Gannet

Funding: The research was financially supported by the Holsworth Wildlife Research Endowment. Acknowledgments We thank the Victorian Marine Science Consortium, Sea All Dolphin Swim, Parks Victoria, and the Point Danger Management Committee for logistical support. We are grateful for the assistance of the many field volunteers involved in the study.Peer reviewedPublisher PD

Ucma/GRP inhibits phosphate-induced vascular smooth muscle cell calcification via SMAD-dependent BMP signalling

Vascular calcification (VC) is the process of deposition of calcium phosphate crystals in the blood vessel wall, with a central role for vascular smooth muscle cells (VSMCs). VC is highly prevalent in chronic kidney disease (CKD) patients and thought, in part, to be induced by phosphate imbalance. The molecular mechanisms that regulate VC are not fully known. Here we propose a novel role for the mineralisation regulator Ucma/GRP (Upper zone of growth plate and Cartilage Matrix Associated protein/Gla Rich Protein) in phosphate-induced VSMC calcification. We show that Ucma/GRP is present in calcified atherosclerotic plaques and highly expressed in calcifying VSMCs in vitro. VSMCs from Ucma/GRP(-/-) mice showed increased mineralisation and expression of osteo/chondrogenic markers (BMP-2, Runx2, beta-catenin, p-SMAD1/5/8, ALP, OCN), and decreased expression of mineralisation inhibitor MGP, suggesting that Ucma/GRP is an inhibitor of mineralisation. Using BMP signalling inhibitor noggin and SMAD1/5/8 signalling inhibitor dorsomorphin we showed that Ucma/GRP is involved in inhibiting the BMP-2-SMAD1/5/8 osteo/chondrogenic signalling pathway in VSMCs treated with elevated phosphate concentrations. Additionally, we showed for the first time evidence of a direct interaction between Ucma/GRP and BMP-2. These results demonstrate an important role of Ucma/GRP in regulating osteo/chondrogenic differentiation and phosphate-induced mineralisation of VSMCs.NWO ZonMw [MKMD 40-42600-98-13007]; FCT [SFRH/BPD/70277/2010]info:eu-repo/semantics/publishedVersio

Susceptibility of hamsters to clostridium difficile isolates of differing toxinotype

Clostridium difficile is the most commonly associated cause of antibiotic associated disease (AAD), which caused ~21,000 cases of AAD in 2011 in the U.K. alone. The golden Syrian hamster model of CDI is an acute model displaying many of the clinical features of C. difficile disease. Using this model we characterised three clinical strains of C. difficile, all differing in toxinotype; CD1342 (PaLoc negative), M68 (toxinotype VIII) and BI-7 (toxinotype III). The naturally occurring non-toxic strain colonised all hamsters within 1-day post challenge (d.p.c.) with high-levels of spores being shed in the faeces of animals that appeared well throughout the entire experiment. However, some changes including increased neutrophil influx and unclotted red blood cells were observed at early time points despite the fact that the known C. difficile toxins (TcdA, TcdB and CDT) are absent from the genome. In contrast, hamsters challenged with strain M68 resulted in a 45% mortality rate, with those that survived challenge remaining highly colonised. It is currently unclear why some hamsters survive infection, as bacterial and toxin levels and histology scores were similar to those culled at a similar time-point. Hamsters challenged with strain BI-7 resulted in a rapid fatal infection in 100% of the hamsters approximately 26 hr post challenge. Severe caecal pathology, including transmural neutrophil infiltrates and extensive submucosal damage correlated with high levels of toxin measured in gut filtrates ex vivo. These data describes the infection kinetics and disease outcomes of 3 clinical C. difficile isolates differing in toxin carriage and provides additional insights to the role of each toxin in disease progression

Intensity modulated radiotherapy in locally advanced thyroid cancer: Outcomes of a sequential phase I dose-escalation study.

BACKGROUND AND PURPOSE:To determine the safety and tolerability of dose-escalation using modestly accelerated IMRT in high-risk locally advanced thyroid cancer requiring post-operative radiotherapy, and to report preliminary data on efficacy. MATERIALS AND METHODS:A sequential Phase I dose-escalation design was used. Dose level one (DL1) received 58.8 Gy/28F to the post-operative bed and 50 Gy/28F to elective nodes. DL2 received 66.6 Gy/30F to the thyroid bed, 60 Gy/30F to post-operative nodal levels and 54 Gy/30F to elective nodal levels. Acute (NCICTCv.2.0) and late toxicities (RTOG and modified LENTSOM) were recorded. The primary endpoint was the number of patients with ≥Grade 3 (G3) toxicity at 12 months post-treatment. RESULTS:Fifteen patients were recruited to DL1 and twenty-nine to DL2. At 12 months ≥G3 toxicities were 8.3% in both DL1 and DL2. At 60 months, ≥G3 toxicity was reported in 3 (33%) patients in DL1 and 1 (7%) in DL2. One patient in DL2 died at 24 months from radiation-induced toxicity. Time to relapse and overall survival rates were higher in DL2, but this was not statistically significant. Dose-escalation using this accelerated regimen can be safely performed with a toxicity profile similar to reported series using conventional doses

Parathyroid autotransplantation in extensive head and neck resections: case series report

Permanent or temporary hypoparathyroidism may be a debilitating result of radical cervical surgery, as noted most commonly following thyroid or parathyroid surgery. However, it can also be the outcome of any surgical procedure involving bilateral extensive manipulation of the anterior neck triangle, especially in order to ensure oncologically adequate surgical margins

Ribosomal oxygenases are structurally conserved from prokaryotes to humans

2-Oxoglutarate (2OG)-dependent oxygenases have important roles in the regulation of gene expression via demethylation of N-methylated chromatin components1,2 and in the hydroxylation of transcription factors3 and splicing factor proteins4. Recently, 2OG-dependent oxygenases that catalyse hydroxylation of transfer RNA5,6,7 and ribosomal proteins8 have been shown to be important in translation relating to cellular growth, TH17-cell differentiation and translational accuracy9,10,11,12. The finding that ribosomal oxygenases (ROXs) occur in organisms ranging from prokaryotes to humans8 raises questions as to their structural and evolutionary relationships. In Escherichia coli, YcfD catalyses arginine hydroxylation in the ribosomal protein L16; in humans, MYC-induced nuclear antigen (MINA53; also known as MINA) and nucleolar protein 66 (NO66) catalyse histidine hydroxylation in the ribosomal proteins RPL27A and RPL8, respectively. The functional assignments of ROXs open therapeutic possibilities via either ROX inhibition or targeting of differentially modified ribosomes. Despite differences in the residue and protein selectivities of prokaryotic and eukaryotic ROXs, comparison of the crystal structures of E. coli YcfD and Rhodothermus marinus YcfD with those of human MINA53 and NO66 reveals highly conserved folds and novel dimerization modes defining a new structural subfamily of 2OG-dependent oxygenases. ROX structures with and without their substrates support their functional assignments as hydroxylases but not demethylases, and reveal how the subfamily has evolved to catalyse the hydroxylation of different residue side chains of ribosomal proteins. Comparison of ROX crystal structures with those of other JmjC-domain-containing hydroxylases, including the hypoxia-inducible factor asparaginyl hydroxylase FIH and histone Nε-methyl lysine demethylases, identifies branch points in 2OG-dependent oxygenase evolution and distinguishes between JmjC-containing hydroxylases and demethylases catalysing modifications of translational and transcriptional machinery. The structures reveal that new protein hydroxylation activities can evolve by changing the coordination position from which the iron-bound substrate-oxidizing species reacts. This coordination flexibility has probably contributed to the evolution of the wide range of reactions catalysed by oxygenases

The puzzle of self-reported weight gain in a month of fasting (Ramadan) among a cohort of Saudi families in Jeddah, Western Saudi Arabia

<p>Abstract</p> <p>Background</p> <p>During Ramadan fast, approximately one billion Muslims abstain from food and fluid between the hours of sunrise to sunset, and usually eat a large meal after sunset and another meal before sunrise. Many studies reported good health-related outcomes of fasting including weight loss. The objective of this study is to identify the local pattern of expenditure on food consumption, dietary habits during Ramadan and correlate that to self-reported weight gain after Ramadan in a group of families in Jeddah, Western Saudi Arabia.</p> <p>Methods</p> <p>A Cross-section study using a pre-designed questionnaire to identify the local pattern of expenditure on food consumption, dietary habits during Ramadan and correlate that to self-reported weight gain after Ramadan in a representative cohort of Saudis living in Jeddah. It was piloted on 173 nutrition students and administered by them to their families.</p> <p>Results</p> <p>A total of 173 Saudi families were interviewed. One out of 5 indicated that their expenditure increases during Ramadan. Approximately two thirds of the respondents (59.5%) reported weight gain after Ramadan. When asked about their perspective explanations for that: 40% attributed that to types of foods being rich in fat and carbohydrates particularly date in (Sunset meal) 97.7% and rice in (Dawn meal) 80.9%. One third (31.2%) indicated that it was due to relative lack of physical exercise in Ramadan and 14.5% referred that to increase in food consumption. Two thirds (65.2%) of those with increased expenditure reported weight gain.</p> <p>Conclusion</p> <p>Surprisingly weight gain and not weight loss was reported after Ramadan by Saudis which indicates timely needed life-style and dietary modification programs for a population which reports one of the highest prevalence rates of diabetes.</p

Endangered edible orchids and vulnerable gatherers in the context of HIV/AIDS in the Southern Highlands of Tanzania

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