84 research outputs found
Temperature evolution of magnetic structure of HoFeO by single crystal neutron diffraction
We have investigated the temperature evolution of the magnetic structures of
HoFeO by single crystal neutron diffraction. The three different magnetic
structures found as a function of temperature for \hfo\ are described by the
magnetic groups Pbn, Pbn and Pbn and are stable in the
temperature ranges 600-55~K, 55-37~K and 35~K respectively. In
all three the fundamental coupling between the Fe sub-lattices remains the same
and only their orientation and the degree of canting away from the ideal axial
direction varies. The magnetic polarisation of the Ho sub-lattices in these two
higher temperature regions, in which the major components of the Fe moment lie
along and , is very small. The canting of the moments from the axial
directions is attributed to the antisymmetric interactions allowed by the
crystal symmetry. They include contributions from single ion anisotropy as well
as the Dzyaloshinski antisymmetric exchange. In the low temperature phase two
further structural transitions are apparent in which the spontaneous
magnetisation changes sign with respect to the underlying antiferromagnetic
configuration. In this temperature range the antisymmetric exchange energy
varies rapidly as the the Ho sub-lattices begin to order. So long as the
ordered Ho moments are small the antisymmetric exchange is due only to Fe-Fe
interactions, but as the degree of Ho order increases the Fe-Ho interactions
take over whilst at the lowest temperatures, when the Ho moments approach
saturation the Ho-Ho interactions dominate. The reversals of the spontaneous
magnetisation found in this study suggest that in \hfo\ the sums of the Fe-Fe
and Ho-Ho antisymmetric interactions have the same sign as one another, but
that of the Ho-Fe terms is opposite
Lightweight asynchronous scheduling in heterogeneous reconfigurable systems
The trend for heterogeneous embedded systems is the integration of accelerators and general-purpose CPU cores on the same die. In these integrated architectures, like the Zynq UltraScale+ board (CPU+FPGA) that we target in this work, hardware support for shared memory and low-overhead synchronization between the accelerator and the CPU cores make the case for exploring strategies that exploit a tight collaboration between the CPUs and the accelerator. In this paper we propose a novel lightweight scheduling strategy, FastFit, targeted to FPGA accelerators, and a new scheduler based on it, named MultiFastFit, which asynchronously tackles heterogeneous systems comprised of a variety of CPU cores and FPGA IPs. Our strategy significantly reduces the overhead to automatically compute the near-optimal chunksizes when compared to a previous state-of-the-art auto-tuned approach, which makes our approach more suitable for fine-grained applications. Additionally, our scheduler MultiFastFit has been designed to enable the efficient co-execution of work among compute devices in such a way that all the devices are busy while minimizing the load unbalance. Our approaches have been evaluated using four benchmarks carefully tuned for the low-power UltraScale+ platform. Our experiments demonstrate that the FastFit strategy always finds the near-optimal FPGA chunksize for any device configuration at a reasonable cost, even for fine-grained and irregular applications, and that heterogeneous CPU+FPGA co-executions that exploit all the compute devices are usually faster and more energy efficient than the CPU-only and FPGA-only executions. We have also compared MultiFastFit with other state-of-the-art scheduling strategies, finding that it outperforms other auto-tuned approach up to 2x and it achieves similar results to manually-tuned schedulers without requiring an offline search of the ideal CPU-FPGA partition or FPGA chunk granularity. © 2022 The Author
Little-Parks effect and multiquanta vortices in a hybrid superconductor--ferromagnet system
Within the phenomenological Ginzburg-Landau theory we investigate the phase
diagram of a thin superconducting film with ferromagnetic nanoparticles. We
study the oscillatory dependence of the critical temperature on an external
magnetic field similar to the Little-Parks effect and formation of multiquantum
vortex structures. The structure of a superconducting state is studied both
analytically and numerically.Comment: 7 pages, 1 figure. Submitted to J. Phys.: Condens. Mat
Mitochondrial and endoplasmic reticulum stress pathways cooperate in zearalenone-induced apoptosis of human leukemic cells
<p>Abstract</p> <p>Background</p> <p>Zearalenone (ZEA) is a phytoestrogen from <it>Fusarium </it>species. The aims of the study was to identify mode of human leukemic cell death induced by ZEA and the mechanisms involved.</p> <p>Methods</p> <p>Cell cytotoxicity of ZEA on human leukemic HL-60, U937 and peripheral blood mononuclear cells (PBMCs) was performed by using 3-(4,5-dimethyl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Reactive oxygen species production, cell cycle analysis and mitochondrial transmembrane potential reduction was determined by employing 2',7'-dichlorofluorescein diacetate, propidium iodide and 3,3'-dihexyloxacarbocyanine iodide and flow cytometry, respectively. Caspase-3 and -8 activities were detected by using fluorogenic Asp-Glu-Val-Asp-7-amino-4-methylcoumarin (DEVD-AMC) and Ile-Glu-Thr-Asp-7-amino-4-methylcoumarin (IETD-AMC) substrates, respectively. Protein expression of cytochrome c, Bax, Bcl-2 and Bcl-xL was performed by Western blot. The expression of proteins was assessed by two-dimensional polyacrylamide gel-electrophoresis (PAGE) coupled with LC-MS2 analysis and real-time reverse transcription polymerase chain reaction (RT-PCR) approach.</p> <p>Results</p> <p>ZEA was cytotoxic to U937 > HL-60 > PBMCs and caused subdiploid peaks and G1 arrest in both cell lines. Apoptosis of human leukemic HL-60 and U937 cell apoptosis induced by ZEA was via an activation of mitochondrial release of cytochrome c through mitochondrial transmembrane potential reduction, activation of caspase-3 and -8, production of reactive oxygen species and induction of endoplasmic reticulum stress. Bax was up regulated in a time-dependent manner and there was down regulation of Bcl-xL expression. Two-dimensional PAGE coupled with LC-MS2 analysis showed that ZEA treatment of HL-60 cells produced differences in the levels of 22 membrane proteins such as apoptosis inducing factor and the ER stress proteins including endoplasmic reticulum protein 29 (ERp29), 78 kDa glucose-regulated protein, heat shock protein 90 and calreticulin, whereas only <it>ERp29 </it>mRNA transcript increased.</p> <p>Conclusion</p> <p>ZEA induced human leukemic cell apoptosis via endoplasmic stress and mitochondrial pathway.</p
Metabolites of Purine Nucleoside Phosphorylase (NP) in Serum Have the Potential to Delineate Pancreatic Adenocarcinoma
Pancreatic Adenocarcinoma (PDAC), the fourth highest cause of cancer related deaths in the United States, has the most aggressive presentation resulting in a very short median survival time for the affected patients. Early detection of PDAC is confounded by lack of specific markers that has motivated the use of high throughput molecular approaches to delineate potential biomarkers. To pursue identification of a distinct marker, this study profiled the secretory proteome in 16 PDAC, 2 carcinoma in situ (CIS) and 7 benign patients using label-free mass spectrometry coupled to 1D-SDS-PAGE and Strong Cation-Exchange Chromatography (SCX). A total of 431 proteins were detected of which 56 were found to be significantly elevated in PDAC. Included in this differential set were Parkinson disease autosomal recessive, early onset 7 (PARK 7) and Alpha Synuclein (aSyn), both of which are known to be pathognomonic to Parkinson's disease as well as metabolic enzymes like Purine Nucleoside Phosphorylase (NP) which has been exploited as therapeutic target in cancers. Tissue Microarray analysis confirmed higher expression of aSyn and NP in ductal epithelia of pancreatic tumors compared to benign ducts. Furthermore, extent of both aSyn and NP staining positively correlated with tumor stage and perineural invasion while their intensity of staining correlated with the existence of metastatic lesions in the PDAC tissues. From the biomarker perspective, NP protein levels were higher in PDAC sera and furthermore serum levels of its downstream metabolites guanosine and adenosine were able to distinguish PDAC from benign in an unsupervised hierarchical classification model. Overall, this study for the first time describes elevated levels of aSyn in PDAC as well as highlights the potential of evaluating NP protein expression and levels of its downstream metabolites to develop a multiplex panel for non-invasive detection of PDAC
Active fixturing: literature review and future research directions
Fixtures are used to fixate, position and support workpieces and represent a crucial tool in manufacturing. Their performance determines the result of the whole manufacturing process of a product. There is a vast amount of research done on automatic fixture layout synthesis and optimisation and fixture design verification. Most of this work considers fixture mechanics to be static and the fixture elements to be passive. However, a new generation of fixtures has emerged that has actuated fixture elements for active control of the part–fixture system during manufacturing operations to increase the end product quality. This paper analyses the latest studies in the field of active fixture design and its relationship with flexible and reconfigurable fixturing systems. First, a brief introduction is given on the importance of research of fixturing systems. Secondly, the basics of workholding and fixture design are visited, after which the state-of-the-art in active fixturing and related concepts is presented. Fourthly, part–fixture dynamics and design strategies which take these into account are discussed. Fifthly, the control strategies used in active fixturing systems are examined. Finally, some final conclusions and prospective future research directions are presented
Oxidative protein labeling in mass-spectrometry-based proteomics
Oxidation of proteins and peptides is a common phenomenon, and can be employed as a labeling technique for mass-spectrometry-based proteomics. Nonspecific oxidative labeling methods can modify almost any amino acid residue in a protein or only surface-exposed regions. Specific agents may label reactive functional groups in amino acids, primarily cysteine, methionine, tyrosine, and tryptophan. Nonspecific radical intermediates (reactive oxygen, nitrogen, or halogen species) can be produced by chemical, photochemical, electrochemical, or enzymatic methods. More targeted oxidation can be achieved by chemical reagents but also by direct electrochemical oxidation, which opens the way to instrumental labeling methods. Oxidative labeling of amino acids in the context of liquid chromatography(LC)–mass spectrometry (MS) based proteomics allows for differential LC separation, improved MS ionization, and label-specific fragmentation and detection. Oxidation of proteins can create new reactive groups which are useful for secondary, more conventional derivatization reactions with, e.g., fluorescent labels. This review summarizes reactions of oxidizing agents with peptides and proteins, the corresponding methodologies and instrumentation, and the major, innovative applications of oxidative protein labeling described in selected literature from the last decade
What have 10 years of health insurance reforms brought about in Bulgaria?: re-appraising the Health Insurance Act of 1998
This article discusses the financial reforms in the Bulgarian public health care sector. Since 1998, when the Bulgarian parliament passed the Health Insurance Act, compulsory contributions for social health insurance have become the main source of health care financing. They replaced the previous tax-based health care funding mechanism. This article reviews empirical evidence and macro indicators to analyse to what extent the expectations of this reform are achieved. Two groups of sources are reviewed: (1) publications prior to the implementation of the social health insurance in Bulgaria that discuss its potential impact; (2) publications after the insurance implementation, that investigate the actual impact of this reform. The results suggest that social health insurance in Bulgaria brought about certain efficiency improvements in the public health care sector. However, the overall social benefit of the reform is doubtful. The main reasons for this are related to the ineffective organisation of the Bulgarian public health care sector, as well as to the overall lack of financial resources for health care in the country
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