53 research outputs found

    Research misconduct in the fields of ethics and philosophy: researchers’ perceptions in Spain

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    This is the Author’s Original Manuscript (AOM) (also called a “preprint”) sent to review to Science and Engineering Ethics on 11/10/2020. The final version of the article was published online at SEE on 21/01/2021. The online version is available at: https://doi.org/10.1007/s11948-021-00278-wEmpirical studies have revealed a disturbing prevalence of research misconduct in a wide variety of disciplines, although not, to date, in the areas of ethics and philosophy. This study aims to provide empirical evidence on perceptions of how serious a problem research misconduct is in these two disciplines in Spain, particularly regarding the effects that the model used to evaluate academics’ research performance may have on their ethical behaviour. The methodological triangulation applied in the study combines a questionnaire, a debate at the annual meeting of scientific association, and in-depth interviews. Of the 541 questionnaires sent out, 201 responses were obtained (37.1% of the total sample), with a significant difference in the participation of researchers in philosophy (30.5%) and in ethics (52.8%); 26 researchers took part in the debate and 14 interviews were conducted. The questionnaire results reveal that 91.5% of the respondents considered research misconduct to be on the rise; 63.2% considered at least three of the fraudulent practices referred to in the study to be commonplace, and 84.1% identified two or more such practices. The researchers perceived a high prevalence of duplicate publication (66.5%) and self-plagiarism (59.0%), use of personal influence (57.5%) and citation manipulation (44.0%), in contrast to a low perceived incidence of data falsification or fabrication (10.0%). The debate and the interviews corroborated these data. Researchers associated the spread of these misconducts with the research evaluation model applied in Spain

    Probenecid Blocks Human P2X7 Receptor-Induced Dye Uptake via a Pannexin-1 Independent Mechanism

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    P2X7 is a ligand-gated ion channel which is activated by ATP and displays secondary permeability characteristics. The mechanism of development of the secondary permeability pathway is currently unclear, although a role for the hemichannel protein pannexin-1 has been suggested. In this study we investigated the role of pannexin-1 in P2X7-induced dye uptake and ATP-induced IL-1β secretion from human monocytes. We found no pharmacological evidence for involvement of pannexin-1 in P2X7-mediated dye uptake in transfected HEK-293 cells with no inhibition seen for carbenoxolone and the pannexin-1 mimetic inhibitory peptide, 10Panx1. However, we found that probenecid inhibited P2X7-induced cationic and anionic dye uptake in stably transfected human P2X7 HEK-293 cells. An IC50 value of 203 μM was calculated for blockade of ATP-induced responses at human P2X7. Probenecid also reduced dye uptake and IL-1β secretion from human CD14+ monocytes whereas carbenoxolone and 10Panx1 showed no inhibitory effect. Patch clamp and calcium indicator experiments revealed that probenecid directly blocks the human P2X7 receptor

    Urine steroid metabolomics for the differential diagnosis of adrenal incidentalomas in the EURINE-ACT study: a prospective test validation study

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    Placing the library at the heart of plagiarism prevention: The University of Bradford experience.

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    yesPlagiarism is a vexed issue for Higher Education, affecting student transition, retention and attainment. This paper reports on two initiatives from the University of Bradford library aimed at reducing student plagiarism. The first initiative is an intensive course for students who have contravened plagiarism regulations. The second course introduces new students to the concepts surrounding plagiarism with the aim to prevent plagiarism breaches. Since the Plagiarism Avoidance for New Students course was introduced there has been a significant drop in students referred to the disciplinary programme. This paper discusses the background to both courses and the challenges of implementation

    Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury

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    Severe pulmonary infection or vigorous cyclic deformation of the alveolar epithelial type I (AT I) cells by mechanical ventilation leads to massive extracellular ATP release. High levels of extracellular ATP saturate the ATP hydrolysis enzymes CD39 and CD73 resulting in persistent high ATP levels despite the conversion to adenosine. Above a certain level, extracellular ATP molecules act as danger-associated molecular patterns (DAMPs) and activate the pro-inflammatory response of the innate immunity through purinergic receptors on the surface of the immune cells. This results in lung tissue inflammation, capillary leakage, interstitial and alveolar oedema and lung injury reducing the production of surfactant by the damaged AT II cells and deactivating the surfactant function by the concomitant extravasated serum proteins through capillary leakage followed by a substantial increase in alveolar surface tension and alveolar collapse. The resulting inhomogeneous ventilation of the lungs is an important mechanism in the development of ventilation-induced lung injury. The high levels of extracellular ATP and the upregulation of ecto-enzymes and soluble enzymes that hydrolyse ATP to adenosine (CD39 and CD73) increase the extracellular adenosine levels that inhibit the innate and adaptive immune responses rendering the host susceptible to infection by invading microorganisms. Moreover, high levels of extracellular adenosine increase the expression, the production and the activation of pro-fibrotic proteins (such as TGF-β, α-SMA, etc.) followed by the establishment of lung fibrosis

    SheddomeDB: the ectodomain shedding database for membrane-bound shed markers

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    Slicing vs. Chunking Product-Harm Crisis: Antecedents and Firm Performance Implications

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    Purpose: The high prevalence of product-harm crises (PHC) represents a continuing challenge to which firms sometimes react by announcing several smaller recalls (i.e. slicing) but at other times by announcing the recall of all faulty products at once (i.e. chunking). The slicing vs chunking phenomenon has not been identified by prior literature; this study aims to explore two research questions: Why do firms sometimes slice and other times chunk PHC? Do slicing and chunking affect firm performance differently? Design/methodology/approach: The authors examined recall guidelines from the US National Highway Traffic Safety Administration (NHTSA) and conducted expert interviews as well as a quantitative analysis of 378 product recalls to determine the antecedents of slicing vs chunking. The authors further performed an event study to examine the impact of slicing vs chunking PHCs on firms’ financial performance. Findings: The authors find that slicing vs chunking is not a deliberate strategy but rather the consequence of firms’ resource availability and constraints. Furthermore, the authors show that larger firms have a lower likelihood of slicing versus chunking. By contrast, larger R&D expenditures, and greater reputation, as well as larger recall sizes, increase the likelihood of slicing versus chunking. Finally, the results reveal that, compared to chunking, slicing PHC has a strong negative impact on firms’ stock value. Research limitations/implications: The authors relied on recalls in the US automobile industry. A possible extension would be to study the same phenomenon in other industries or other geographical areas. In addition, the results need to be generalized to other types of negative news that can be either decoupled (slicing) or coupled (chunking), especially negative news for which firms have more discretion regarding the timing of their announcements than for product recalls. Practical implications: As shown by prior research (Eilert et al., 2017), firms should aim to announce recalls quickly in the wake of a PHC. Importantly though, the results indicate that speed should not come at the expense of comprehensiveness in identifying all defective products, so that only one recall is needed. As suggested by our findings about PHC, investors may react negatively to the slicing of other types of negative news; thus, the results suggest how to best communicate to external stakeholders during crises in general. Originality/value: To the best of the authors’ knowledge, this is the first study that examines why firms sometimes slice and at other times chunk PHC and identifies the performance implications of these two types of recalls in response to PHC
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