Miracle-dz/UniFAR-FTUs huggingface dataset:
Wide-band EM characterization of a Ni-Zn ferrite tile in a TEM structure

This paper presents an original wide-band method (from 1 MHz to 1 GHz in the paper) for the electromagnetic (EM) characterization of a Ni-Zn ferrite tile. The method requires the S-parameter measurements of a TEM structure (a stripline cell in this paper) without and with the sample under test (SUT). In parallel, the experiment is faithfully reproduced by simulation through the FDTD method for both cases. This enables to determine the electromagnetic properties of the SUT by adjusting its properties in simulation in order to match the measured S-parameters of the stripline cell thanks to an optimization process. The main advantage of the proposed method lies in the fact that no machining process of the sample is required provided that 1) the size of the sample enables to insert it within the stripline structure, 2) the position of the SUT in the propagating device is known accurately and 3) the insertion of the SUT sufficiently modifies the S-parameters of the TEM structure. Experimental results obtained on a ferrite tile are provided showing excellent agreements with results given in the literature.
Determination of phytic acid and inositolphosphates in barley

Phytic acid (PA) and lower inositolphosphates (InsPn) is the main storage form of phosphorus in grains or seeds. The content of PA and InsPn in different varieties of barley was analyzed by capillary isotachophoresis and online‐coupled capillary isotachophoresis with CZE. The electrolytes (in demineralized water) for the isotachophoretic analysis consisted of 10 mM HCl, 14 mM glycylglycine, and 0.1% 2‐hydroxyethylcellulose (leading) and 10 mM citric acid (terminating). The optimized electrolytes for the online coupling isotachophoresis with zone electrophoresis analysis were mixtures of 5 mM HCl, 7 mM glycylglycine, and 0.1% 2‐hydroxyethylcellulose (leading), 20 mM citric acid, 10 mM glycylglycine, and 0.1% 2‐hydroxyethylcellulose (background) and 10 mM citric acid (terminating). PA and all studied InsPn were separated within 25 min and detected by a conductivity detector. Simple sample preparation (acidic extraction), sufficient sensitivity, speed of analysis, and low running cost are important attributes of the electrophoretic methods. The method was used for the determination of PA and InsPn in barley varieties within an ongoing research project.
The chemistry of the S-nitrosoglutathione/glutathione system.

S-Nitrosothiols have generated considerable interest due to their ability to act as nitric oxide (NO) donors and due to their possible involvement in bioregulatory systems-e.g., NO transfer reactions. Elucidation of the reaction pathways involved in the modification of the thiol group by S-nitrosothiols is important for understanding the role of S-nitroso compounds in vivo. The modification of glutathione (GSH) in the presence of S-nitrosoglutathione (GSNO) was examined as a model reaction. Incubation of GSNO (1 mM) with GSH at various concentrations (1-10 mM) in phosphate buffer (pH 7.4) yielded oxidized glutathione, nitrite, nitrous oxide, and ammonia as end products. The product yields were dependent on the concentrations of GSH and oxygen. Transient signals corresponding to GSH conjugates, which increased by one mass unit when the reaction was carried out with 15N-labeled GSNO, were identified by electrospray ionization mass spectrometry. When morpholine was present in the reaction system, N-nitrosomorpholine was formed. Increasing concentrations of either phosphate or GSH led to lower yields of N-nitrosomorpholine. The inhibitory effect of phosphate may be due to reaction with the nitrosating agent, nitrous anhydride (N2O3), formed by oxidation of NO. This supports the release of NO during the reaction of GSNO with GSH. The products noted above account quantitatively for virtually all of the GSNO nitrogen consumed during the reaction, and it is now possible to construct a complete set of pathways for the complex transformations arising from GSNO + GSH.
Effects of exposure to low pH on the lateral mobility of influenza hemagglutinin expressed at the cell surface: correlation between mobility inhibition and inactivation.

To investigate the possible role of viral glycoprotein mobility in membrane fusion, fluorescence photobleaching recovery was employed to study the effects of exposure to mildly acidic pH (required to convert many viral fusion proteins to the fusion-active form) on the lateral mobility of influenza hemagglutinin (HA) proteins expressed at the surface of transfected cells. HA proteins from two different strains were compared: X:31 HA, which is activated by a brief exposure to pH 4.9 but is irreversibly inactivated at longer exposure times, and HA from A/Japan/305/57, which is relatively stable to inactivation at this pH [Puri, A. , Booy, F.P., Doms, R.W. , White, J.M. , & Blumenthal, R. (1990) J. Virol. 64, 3824-3832]. The HA proteins from both strains, expressed in CV-1 cells using VS-40 vectors, exhibited relatively unrestricted lateral diffusion at the cell surface. The high mobility persisted following a brief exposure (1 min) to pH 4.9 to mediate conversion to the fusogenic state. Longer times (up to 15 min) of preincubation at pH 4.9 inhibited the lateral mobility of X:31 HA (the lateral diffusion rate was markedly reduced, followed by immobilization) but not of A/Japan HA, whose fusion activity is resistant to such treatment. Inhibition of the lateral mobility of X:31 HA due to preincubation at low pH was not specific to the CV-1 cells and was found also in a CHO cell line stably expressing this protein. The results presented demonstrate a close correlation between loss of mobility and inactivation of fusogenic activity, in accord with the notion that lateral motion of the HA proteins is required for fusion. (ABSTRACT TRUNCATED AT 250 WORDS)
Association of NFKB1 and NFKBIA Polymorphisms in Relation to Susceptibility of Behçet's Disease

Behçet's disease (BD) is a chronic inflammatory autoimmune disease. Although raised levels of proinflammatory cytokines in BD have been reported, the pathogenesis is still unknown. The aim of this study was to investigate the association of NFKB1 and NFKBIA polymorphisms and their single and combined analysis effects on susceptibility of BD in Turkish population. We analysed the distribution of NFKB1 ‐94 ins/del ATTG (rs28362491) and NFKBIA 3′ UTR A→G (rs696) polymorphisms using PCR‐RFLP method in 89 patients with BD and 190 controls in this population. Statistical analysis of the results was performed by calculating OR, and 95% CI via χ2 test and using Bonferroni correction. According to the significant results of both single and combined genotype analysis, the frequencies of ins/ins genotype and ins allele of rs28362491 were significantly higher in patients with BD (Pc = 0.003, 0.004, respectively). Also, higher frequencies of the rs696 variant containing AA genotype was found in patients with BD (Pc = 0.0033), whereas no statistical significant differences in distribution of the alleles of rs696 polymorphism in patients and controls. In addition, according to the combined genotype analysis, the wild type of both rs28362491 and rs696 polymorphisms (ins/ins/AA genotype) was also significantly higher in BD cases (Pc = 0.044). Our findings prove that both single and combined genotype analysis of rs28362491 and rs696 polymorphisms indicate that the wild genotypes of both two SNPs (ins/ins and AA genotypes) and ins/ins/AA combined genotype are strongly associated with enhanced risk of BD in a Turkish population.
The evolution of a complex trait: cuticular hydrocarbons in ants evolve independent from phylogenetic constraints

Cuticular hydrocarbons (CHCs) are ubiquitous and highly diverse in insects, serving as communication signal and waterproofing agent. Despite their vital function, the causes, mechanisms and constraints on CHC diversification are still poorly understood. Here, we investigated phylogenetic constraints on the evolution of CHC profiles, using a global data set of the species‐rich and chemically diverse ant genus Crematogaster. We decomposed CHC profiles into quantitative (relative abundances, chain length) and qualitative traits (presence/absence of CHC classes). A species‐level phylogeny was estimated using newly generated and previously published sequences from five nuclear markers. Moreover, we reconstructed a phylogeny for the chemically diverse Crematogaster levior species group using cytochrome oxidase I. Phylogenetic signal was measured for these traits on genus and clade level and within the chemically diverse C. levior group. For most quantitative CHC traits, phylogenetic signal was low and did not differ from random expectation. This was true on the level of genus, clade and species group, indicating that CHC traits are evolutionary labile. In contrast, the presence or absence of alkenes and alkadienes was highly conserved within the C. levior group. Hence, the presence or absence of biosynthetic pathways may be phylogenetically constrained, especially at lower taxonomic levels. Our study shows that CHC composition can evolve rapidly, allowing insects to quickly adapt their chemical profiles to external selection pressures, whereas the presence of biosynthetic pathways appears more constrained. However, our results stress the importance to consider the taxonomic level when investigating phylogenetic constraints.
CD4+ T-cell population mediates development of inflammatory bowel disease in T-cell receptor alpha chain-deficient mice.

BACKGROUND & AIMS Increase of T cells expressing CD4 and T-cell receptor (TCR) alpha- beta+ (beta[dim]) was observed in the mucosal and peripheral lymphoid tissues of TCR alpha-/- mice with inflammatory bowel disease (IBD). The aim of this study was to characterize the CD4+ TCR alpha-beta+ T cells. METHODS Cytokine production, TCR V beta usage, and helper function for Peyer's patch B cells by the CD4+ TCR alpha-beta+ T cells were assessed. RESULTS The CD4+ TCR alpha-beta+ T cells purified from mesenteric lymph nodes and lamina propria of the intestine of IBD mice exclusively produced interleukin 4, used selected subsets (V beta6, V beta8, V beta14, and V beta15) of TCR, and massively proliferated after stimulation with staphylococcal enterotoxin B. Addition of the CD4+ TCR alpha-beta+ T cells to Peyer's patch B-cell cultures markedly enhanced immunoglobulin (Ig) A, IgG, and IgM antibody responses. Furthermore, depletion of the TCR alpha-beta+ T cells with monoclonal antibody against TCR beta chain completely suppressed the onset of IBD and polyclonal B-cell activation in the TCR alpha-/- mice. CONCLUSIONS These findings suggest the CD4+ TCR alpha-beta+ T cells-mediated development of IBD in TCR alpha-/- mice.
The Use of 18F-FDG PET in the Diagnosis of Cardiac Sarcoidosis: A Systematic Review and Metaanalysis Including the Ontario Experience

Cardiac sarcoidosis is a potentially fatal complication of sarcoidosis. The 1993 guidelines of the Ministry of Health, Labour, and Welfare (MHLW) of Japan have been used as the diagnostic gold standard and for comparison with imaging modalities. 18F-FDG PET is not currently included in the guidelines. However, studies have shown promising data using 18F-FDG PET. We conducted a systematic review of studies that evaluated the accuracy of 18F-FDG PET for the diagnosis of cardiac sarcoidosis compared with MHLW guidelines. Data from a prospective Ontario provincial registry are also reported and included in the metaanalysis. Methods: PubMed, Embase, and the Cochrane Central Register of Controlled Trials were searched for studies that satisfied predetermined criteria. Quality evaluation using the Quality Assessment for Diagnostic Accuracy Studies was performed by 2 independent masked observers. Data were extracted and analyzed to measure study-specific and pooled accuracy for 18F-FDG PET compared with the MHLW as the reference. Results: A total of 519 titles was identified; 7 studies, including the Ontario registry, were selected for inclusion. Metaanalysis of these 7 studies was conducted, with a total of 164 patients, most of whom had been diagnosed with systemic sarcoidosis. The prevalence of cardiac sarcoidosis was 50% in the whole population. Pooled estimates for 18F-FDG PET yielded 89% sensitivity (95% confidence interval [CI], 79%–96%), 78% specificity (95% CI, 68%–86%), a 4.1 positive likelihood ratio (95% CI, 1.7–10), and a 0.19 negative likelihood ratio (95% CI, 0.1–0.4). The overall diagnostic odds ratio was 25.6 (95% CI, 7.3–89.5), and the area under the summary receiver operator characteristic curve was 93% ± 3.5. The Ontario study yielded sensitivity and specificity of 79% and 70%, respectively. Conclusion: The high diagnostic accuracy determined for 18F-FDG PET in this metaanalysis suggests potential value for diagnosis of cardiac sarcoidosis compared with the MHLW guidelines. These results may affect patient care by providing supportive evidence for more effective use of 18F-FDG PET in the diagnosis of cardiac sarcoidosis. Large-scale multicenter studies are required to further evaluate this role.
Cross Project Software Fault Prediction at Design Phase

— Software fault prediction models are created by using the source code, processed metrics from the same or previous version of code and related fault data. Some company do not store and keep track of all artifacts which are required for software fault prediction. To construct fault prediction model for such company, the training data from the other projects can be one potential solution. Earlier we predicted the fault the less cost it requires to correct. The training data consists of metrics data and related fault data at function/module level. This paper investigates fault predictions at early stage using the cross-project data focusing on the design metrics. In this study, empirical analysis is carried out to validate design metrics for cross project fault prediction. The machine learning techniques used for evaluation is Naïve Bayes. The design phase metrics of other projects can be used as initial guideline for the projects where no previous fault data is available. We analyze seven datasets from NASA Metrics Data Program which offer design as well as code metrics. Overall, the results of cross project is comparable to the within company data learning.
The Campylobacter jejuni dccRS two‐component system is required for optimal in vivo colonization but is dispensable for in vitro growth

A Campylobacter jejuni two‐component signal transduction system (TCSTS), designated dccR‐dccS (diminished capacity to colonize; Cj1223c‐Cj1222c), has been found to be important for in vivo colonization but dispensable for in vitro growth. A ΔdccR response regulator mutant generated using the virulent strain 81–176 background exhibited significantly reduced colonization of immunocompetent limited flora (I‐LF) mice, severe combined immunodeficient limited flora (SCID‐LF) mice, and 1‐day‐old chicks. A ΔdccS sensor kinase mutant was likewise defective for colonization in the I‐LF mouse model. ΔdccR‐infected SCID‐LF mice also exhibited dramatically reduced inflammation relative to wild type‐infected SCID‐LF mice. Despite this diminished colonization capacity, the ΔdccRS mutants were indistinguishable from wild type for growth under numerous in vitro conditions as well as for various phenotypes. Microarray analysis identified several genes encoding putative periplasmic and membrane proteins as being regulated by this two‐component system; binding of purified His‐tagged DccR to the promoter region of two of these genes supports a direct protein–DNA interaction. A conserved repeat sequence was identified in the promoter regions of these genes and in three other promoter regions in the genome, including that of an operon encoding a putative type I secretion system. Two of the regulated target genes were found to be essential for optimal colonization. Both the two‐component system and the putative regulated genes have uncharacterized homologues in other Campylobacter and Helicobacter spp. , suggesting that they may perform an important function in colonization among a variety of related pathogenic species.
The transcriptional activator ClgR controls transcription of genes involved in proteolysis and DNA repair in Corynebacterium glutamicum

Expression of the structural genes encoding the ATP‐dependent proteases ClpCP and Lon in Corynebacterium glutamicum and Streptomyces lividans is activated by the transcriptional regulator ClgR in response to yet unknown environmental stimuli. As it was not known whether ClgR controls expression of additional genes we used DNA microarrays in order to comprehensively define the ClgR regulon in C. glutamicum. The mRNA levels of 16 genes decreased ≥ 2‐fold in a ΔclgRΔclpC mutant (ClgR absent) compared with a ΔclpC mutant (ClgR present). For five genes in four operons (NCgl0748, ptrB, hflX and NCgl0240‐recR) regulation by ClgR could be independently verified by primer extension analyses and confirmation of binding of purified ClgR to the regulatory regions of these operons. ptrB encodes an endopeptidase, which is consistent with the proteolytic functions of the genes already known to be under ClgR control. However, RecR is unrelated to proteolysis but required for recombinational repair of UV‐induced DNA damage. Possibly ClgR‐dependent activation of gene expression is triggered by environmental stresses damaging both proteins and nucleic acids, although DNA damage induced by UV radiation and mitomycin C treatment did not result in ClgR‐dependent transcriptional activation of any of the newly identified ClgR regulon members. In order to functionally analyse the NCgl0748 and hflX genes we have constructed C. glutamicum strains with deletions in these genes. The ΔNCgl0748 mutant displayed reduced growth rates in minimal and rich media. The NCgl0748 protein was shown to be localized in the cytoplasm only, while the HflX pool is equally distributed between cytoplasm and plasma membrane. In order to study the proposed degradation of ClgR by ClpCP we have constructed a conditional clpP1P2 mutant. Depletion of ClpP1 and ClpP2 in that strain resulted in the accumulation of ClgR, indicating that ClgR is in fact a substrate of the ClpCP1 and/or ClpCP2 protease in C. glutamicum.
Chromosome mapping of the human genes encoding the MAP kinase kinase MEK1 (MAP2K1) to 15q21 and MEK2 (MAP2K2) to 7q32

Activation of the ERK mitogen-activated protein (MAP) kinase pathway has been implicated in the regulation of cell growth, differentiation and senescence. In this pathway, the MAP kinases ERK1/ERK2 are phosphorylated and activated by the dual-specificity kinases MEK1 and MEK2, which in turn are activated by serine phosphorylation by a number of MAP kinase kinase kinases. We report here the chromosomal localization of the human genes encoding the MAP kinase kinase isoforms MEK1 and MEK2. Using a combination of fluorescence in situ hybridization, somatic cell hybrid analysis, DNA sequencing and yeast artificial chromosome (YAC) clone analysis, we have mapped the MEK1 gene (MAP2K1) to chromosome 15q21. We also present evidence for the presence of a MEK1 pseudogene on chromosome 8p21. The MEK2 gene (MAP2K2) was mapped to chromosome 7q32 by fluorescence in situ hybridization and YAC clone analysis.
Impact of Patient Reimbursement Timing and Patient Out-of-Pocket Expenses on Medication Adherence in Patients Covered by Private Drug Insurance Plans

BACKGROUND: Adherence to prescribed medications used in the treatment of chronic diseases is suboptimal, and drug insurance plans can have an impact on adherence. There is little evidence on the impact of patient reimbursement timing on medication adherence. OBJECTIVE: To compare adherence to prescribed medications in privately insured patients from Quebec, Canada, with different patient reimbursement timing and levels of patient out-of-pocket expenses. METHODS: A retrospective cohort was constructed by selecting privately insured patients aged 18-64 years from the reMed database (2008-2012) who filled at least 1 prescription for a medication belonging to 1 of the 10 most prescribed drug classes for chronic diseases. Patient reimbursement timing was classified as immediate (immediate patient reimbursement at the point of service of the portion of the medication cost covered by the insurer) or deferred (patient reimbursement at a later time). Patient outof-pocket expenses related to the medication under study at cohort entry (available only for the immediate patient reimbursement group), which included the deductible and the coinsurance, were categorized into 5 levels (null category and quartiles): $0, $0.01-$3.59, $3.60-$8.11, $8.12-$14.40, and $14.41-$89.99. Adherence was measured with the proportion of days covered (PDC) over 1 year among new users of the medication under study. Linear regression models were used to estimate the adjusted mean difference of PDC between groups. RESULTS: There was no difference in medication adherence between the immediate (n = 1,345) and deferred patient reimbursement (n = 437; difference, 0.0%; 95% CI, -3.0 to 3.0). Patients with the highest patient out-of-pocket expenses were less adherent than those with the lowest patient out-of-pocket expenses (difference, -19.0%; 95% CI, -24.0 to -13.0); however, patients with no patient out-of-pocket expenses were less adherent than those with low patient out-of-pocket expenses (difference, -9.0%; 95% CI, -15.0 to -2.0). CONCLUSIONS: Medication adherence appeared to be unaffected by patient reimbursement timing but was affected by the level of patient out-of-pocket expenses. The absence of a correlation between medication adherence and timing of patient reimbursement might be explained by the relatively rapid reimbursement of expenses by insurance companies in Canada. Subjects with no patient out-of-pocket expenses at the point of service might be less adherent because they place less value on their medications than do patients who must pay even a small amount.
Kelly West Lecture 1991 Challenges in Diabetes Epidemiology—From West to the Rest

The application of epidemiology to the study of non-insulin-dependent diabetes mellitus (NIDDM) is providing new insights into many aspects of this major public-health problem, including its natural history, prevalence, incidence, morbidity, and mortality in diverse populations around the globe. The main impetus came from the late Kelly West's book Epidemiology of Diabetes and its Vascular Lesions. These studies are providing direction for research into the possible moleculardefect or defects and biochemical mechanism or mechanisms underlying NIDDM and important information on the extrinsic (social, cultural, environmental) risk determinants. Studies have highlighted the importance of regional adipose tissue distribution, particularly upper-body obesity, and physical inactivity in enhancing risk of NIDDM. These findings have important implications for the primary prevention of NIDDM, particularly in populations with increased genetic susceptibility such as Polynesians, Micronesians, American and Asian Indians, Mexican Americans, and Australian aborigines.