14 research outputs found

    Magnetic and structural properties of barium hexaferrite BaFe12O19 from various growth techniques

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    Barium hexaferrite powder samples with grains in the m-range were obtained from solid-state sintering, and crystals with sizes up to 5 mm grown from PbO, Na2CO3, and BaB2O4 fluxes, respectively. Carbonate and borate fluxes provide the largest and structurally best crystals at significantly lower growth temperatures of 1533 K compared to flux-free synthesis (1623 K). The maximum synthesis temperature can be further reduced by the application of PbO-containing fluxes (down to 1223 K upon use of 80 at % PbO), however, Pb-substituted crystals Ba1-xPbxFe12O19 with Pb contents in the range of 0.23(2) x 0.80(2) form, depending on growth temperature and flux PbO content. The degree of Pb-substitution has only a minor influence on unit cell and magnetic parameters, although the values for Curie temperature, saturation magnetization, as well as the coercivity of these samples are significantly reduced in comparison with those from samples obtained from the other fluxes. Due to the lowest level of impurities, the samples from carbonate flux show superior quality compared to materials obtained using other methods

    Large expert-curated database for benchmarking document similarity detection in biomedical literature search

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    Document recommendation systems for locating relevant literature have mostly relied on methods developed a decade ago. This is largely due to the lack of a large offline gold-standard benchmark of relevant documents that cover a variety of research fields such that newly developed literature search techniques can be compared, improved and translated into practice. To overcome this bottleneck, we have established the RElevant LIterature SearcH consortium consisting of more than 1500 scientists from 84 countries, who have collectively annotated the relevance of over 180 000 PubMed-listed articles with regard to their respective seed (input) article/s. The majority of annotations were contributed by highly experienced, original authors of the seed articles. The collected data cover 76% of all unique PubMed Medical Subject Headings descriptors. No systematic biases were observed across different experience levels, research fields or time spent on annotations. More importantly, annotations of the same document pairs contributed by different scientists were highly concordant. We further show that the three representative baseline methods used to generate recommended articles for evaluation (Okapi Best Matching 25, Term Frequency-Inverse Document Frequency and PubMed Related Articles) had similar overall performances. Additionally, we found that these methods each tend to produce distinct collections of recommended articles, suggesting that a hybrid method may be required to completely capture all relevant articles. The established database server located at https://relishdb.ict.griffith.edu.au is freely available for the downloading of annotation data and the blind testing of new methods. We expect that this benchmark will be useful for stimulating the development of new powerful techniques for title and title/abstract-based search engines for relevant articles in biomedical research.Peer reviewe

    Prooxidant properties of p66shc are mediated by mitochondria in human cells.

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    p66shc is a protein product of an mRNA isoform of SHC1 gene that has a pro-oxidant and pro-apoptotic activity and is implicated in the aging process. Mitochondria were suggested as a major source of the p66shc-mediated production of reactive oxygen species (ROS), although the underlying mechanisms are poorly understood. We studied effects of p66shc on oxidative stress induced by hydrogen peroxide or by serum deprivation in human colon carcinoma cell line RKO and in diploid human dermal fibroblasts (HDFs). An shRNA-mediated knockdown of p66shc suppressed and an overexpression of a recombinant p66shc stimulated the production of ROS in the both models. This effect was not detected in the mitochondrial DNA-depleted ρ0-RKO cells that do not have the mitochondrial electron transport chain (ETC). The p66shc-dependent accumulation of mitochondrial ROS was detected with HyPer-mito, a mitochondria-targeted fluorescent protein sensor for hydrogen peroxide. The fragmentation of mitochondria induced by mitochondrial ROS was significantly reduced in the p66shc deficient RKO cells. Mitochondria-targeted antioxidants SkQ1 and SkQR1 also decreased the oxidative stress induced by hydrogen peroxide or by serum deprivation. Together the data indicate that the p66shc-dependant ROS production during oxidative stress has mitochondrial origin in human normal and cancer cells

    Pro-oxidant properties of p66shc are inhibited in RKO ρ0 cells.

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    <p>(A) Cell viability was measured after exposure to hydrogen peroxide for 20 hrs at indicated concentrations. (B) DCF-DA fluorescence level in cells after exposure to hydrogen peroxide for 3 hrs at indicated concentrations. Grey columns correspond to cells transduced with control shRNA (sh-C); black columns correspond to cells that express shRNAp66. Represented are the fluorescence intensity values (cell viability) that are measured in three (five) parallel cell cultures. Data were replicated in three independent experiments.</p

    p66shc knockdown decreases but the overexpression auguments the oxidative stress induced by hydrogen peroxide in RKO cells and in HDFs.

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    <p>(A) DCF-DA fluorescence level in RKO cells after an exposure to hydrogen peroxide for 3 hrs at the indicated concentrations. (B) Viability of RKO cells was measured after exposure to hydrogen peroxide (1200 µmol) for 20 hrs. (C) DCF-DA fluorescence level in HDFs after exposure to hydrogen peroxide for 3 hrs at indicated concentrations. Grey columns correspond to cells transduced with control random shRNA (sh-C); black columns correspond to cells that express shRNAp66; grey diagonal hatched columns – cells expressing control empty vector and light diagonal hatched columns refer to cells that overexpress p66shc. Mean values of DCF fluorescence intensity (viability) that are measured in three (five) parallel cell cultures are represented. *p<0.05; **p<0.01 in paired t-test. Data were replicated in three independent experiments.</p

    Genetic knockdown of p66shc and preincubation with SkQ1 prevents fragmentation of mitochondria induced by hydrogen peroxide in RKO cells.

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    <p>Fragmentation of mitochondria in different sublines of RKO cells after exposure to hydrogen peroxide for 20(sh-C); black columns correspond to cells that express shRNAp66, hatched columns – cells transduced with control shRNA and preincubated with 2 nM SkQ1 for 24 hours. Mean and standard deviation values are provided. *p<0.05; **p<0.01 in paired t-test. Data were replicated in three independent experiments.</p

    Mitochondria-targeted antioxidants decrease intracellular and mitochondrial ROS induced by serum deprivation in RKO cells and in HDFs.

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    <p>RKO cells and HDFs were incubated with indicated concentrations of SkQ1 or SkQR1 for 3 days. Quantification of DCF-DA fluorescence was performed in control RKO cells (A) and HDFs (B) and in cells cultivated in a serum free medium for 24 hours and pretreated with different concentrations of SkQ1 and SkQR1. Cells that express HyPer-mito were preincubated with indicated concentrations of SkQ1 or SkQR1. Amplification of HyPer-mito fluorescence was shown in (C) RKO cells, (D) HDFs after cultivation in serum-free medium during 24 hours. Represented are DCF-DA fluorescence and amplification of HyPer-mito fluorescence in three parallel cell cultures, *p<0.05; **p<0.01 in paired t-test. Data were replicated in three independent experiments.</p

    p66shc knockdown inhibits mitochondrial ROS production induced by serum deprivation in RKO cells.

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    <p>(A) DCF-DA fluorescence level in RKO and RKO ρ0 cells in standard media after an incubation in a serum free medium for 24 hrs. (B) Amplification of HyPer-mito fluorescence in RKO cells after an incubation in a serum-free medium for 24 hrs. Grey columns correspond to RKO cells transduced with a control shRNA (sh-C); black columns – RKO cells that express shRNAp66; grey diagonal hatched columns – RKO ρ0 cells expressing control empty vector and light diagonal hatched columns refer to RKO ρ0 cells that express shRNAp66. Represented are DCF-DA fluorescence and amplification of HyPer-mito fluorescence in three parallel cell cultures,*p<0.05; **p<0.01 in paired t-test. Data were replicated in two independent experiments.</p

    Western analysis of <i>SHC1</i> gene products in human colon carcinoma derived cell line RKO and in normal human dermal fibroblasts (HDFs).

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    <p>(A) RKO cells; (B) mitochondria-depleted ρ0 RKO cells; (C) HDFs. The cell lines were infected with either control lentiviral vector expressing random shRNA (shRNA-C), or with a lentiviral construct expressing shRNA against CH2 domain of p66shc (shRNAp66). (D) RKO cells and (E) HDFs, control (Vector) or with introduced lentiviral construct overexpressing recombinant p66shc (rec-p66).</p
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