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Träfflista för sökning "WFRF:(Dehlendorff Christian) srt2:(2008)"

Sökning: WFRF:(Dehlendorff Christian) > (2008)

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1.
  • Dehdarirad, Tahereh, 1984, et al. (författare)
  • Gender differences in citation sentiment: A case study in Life Sciences and Biomedicine
  • 2022
  • Ingår i: Journal of Information Science. - 0165-5515. ; , s. 1-13
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study we investigated whether female and male authors in the field of life sciences and biomedicine differed in their tendency for citation and citation sentiment. The data comprised two sets, cited set and citing set. Cited set comprised 17,237 articles whereas citing set comprised 115,935 articles. The cited set which is from the area Life Sciences & Biomedicine and published during 2012– 2016 was retrieved from the Web of Science Medline. The citing set and its citation contexts wereretrieved using Colil database. The analysis was done using a combination of homophily analysis, regression analysis and a chi-squared test. The covariates in the regression analyses were features related to authors, journal, institution, country, and abstract readability. The homophily analysis showed a significant tendency for female (8%) and male (14%) authorship teams to cite papers by the same gender composition teams. Additionally, the results of regression analysis (Model 1) and pairwise comparisons showed that male authored papers received a significant higher positive sentiment compared to female authored papers. The results of regression analysis (Model 2) showed a small significant positive association between gender similarity of cited and citing authorship teams and the sentiment score. However, further analysis using the chi-squared test showed a significant lower tendency for women to use positive terms when citing the research findings of papers with the same gender composition. Men, in contrast, used significantly more positive terms when citing papers with the same gender composition. Finally, lay summary for a cited paper, country similarity and the venue of cited publication when it was a mega journal had a positive significant association with the sentiment score received.
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2.
  • Tian, Fei, 1964, et al. (författare)
  • Protein disulfide isomerase increases in myocardial endothelial cells in mice exposed to chronic hypoxia: a stimulatory role in angiogenesis.
  • 2009
  • Ingår i: American Journal of Physiology. Heart and Circulatory Physiology. - 1522-1539. ; 297:3, s. H1078-H1086
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous studies have shown that exposure to chronic hypoxia protects against myocardial infarction, but little is known about the cellular and molecular mechanisms involved. Here we observed that chronic hypoxia for 3 wk resulted in improved survival of mice (from 64% to 83%), reduced infarction size (from 45 +/- 4% to 32 +/- 4%, P < 0.05), increased cardiac ejection fraction (from 19 +/- 4% to 35 +/- 5%, P < 0.05), coronary flow velocity under adenosine-induced hyperemia (from 58 +/- 2 to 75 +/- 5 cm/s, P < 0.05), myocardial capillary density (from 3,772 +/- 162 to 4,760 +/- 197 capillaries/mm(2), P < 0.01), and arteriolar density (from 8.04 +/- 0.76 to 10.34 +/- 0.69 arterioles/mm(2), P < 0.05) 3 wk after myocardial infarction. With two-dimensional gel electrophoresis, we identified that protein disulfide isomerase (PDI) was highly upregulated in hypoxic myocardial capillary endothelial cells. The loss of PDI function in endothelial cells by small interfering RNA significantly increased the number of apoptotic cells (by 3.4-fold at hypoxia, P < 0.01) and reduced migration (by 52% at hypoxia, P < 0.001) and adhesion to collagen I (by 42% at hypoxia, P < 0.01). In addition, the specific inhibition of PDI by PDI small interfering RNA (by 46%, P < 0.01) and bacitracin (by 72%, P < 0.001) reduced the formation of tubular structures by endothelial cells. Our data indicate that chronic hypoxic exposure improves coronary blood flow and protects the myocardium against infarction. These beneficial effects may be partly explained by the increased endothelial expression of PDI, which protects cells against apoptosis and increases cellular migration, adhesion, and tubular formation. The increased PDI expression in endothelial cells may be a novel mechanism to protect the myocardium against myocardial ischemic diseases.
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