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Träfflista för sökning "WFRF:(Lasselin Julie) srt2:(2018)"

Sökning: WFRF:(Lasselin Julie) > (2018)

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  • Axelsson, John, et al. (författare)
  • Identification of acutely sick people and facial cues of sickness
  • 2018
  • Ingår i: Proceedings of the Royal Society of London. Biological Sciences. - : The Royal Society. - 0962-8452 .- 1471-2954. ; 285:1870
  • Tidskriftsartikel (refereegranskat)abstract
    • Detection and avoidance of sick individuals have been proposed as essential components in a behavioural defence against disease, limiting the risk of contamination. However, almost no knowledge exists on whether humans can detect sick individuals, and if so by what cues. Here, we demonstrate that untrained people can identify sick individuals above chance level by looking at facial photos taken 2 h after injection with a bacterial stimulus inducing an immune response (2.0 ng kg-1 lipopolysaccharide) or placebo, the global sensitivity index being d' = 0.405. Signal detection analysis (receiver operating characteristic curve area) showed an area of 0.62 (95% confidence intervals 0.60-0.63). Acutely sick people were rated by naive observers as having paler lips and skin, a more swollen face, droopier corners of the mouth, more hanging eyelids, redder eyes, and less glossy and patchy skin, as well as appearing more tired. Our findings suggest that facial cues associated with the skin, mouth and eyes can aid in the detection of acutely sick and potentially contagious people.
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  • Göranson, Sofie Paues, et al. (författare)
  • Circulating H3Cit is elevated in a human model of endotoxemia and can be detected bound to microvesicles
  • 2018
  • Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 8
  • Tidskriftsartikel (refereegranskat)abstract
    • Early diagnosis of sepsis is crucial since prompt interventions decrease mortality. Citrullinated histone H3 (H3Cit), released from neutrophil extracellular traps (NETs) upon binding of platelets to neutrophils following endotoxin stimulation, has recently been proposed a promising blood biomarker in sepsis. Moreover, microvesicles (MVs), which are released during cell activation and apoptosis and carry a variety of proteins from their parental cells, have also been shown to be elevated in sepsis. In a randomized and placebo-controlled human model of endotoxemia (lipopolysaccharide injection; LPS), we now report significant LPS-induced elevations of circulating H3Cit in 22 healthy individuals. We detected elevations of circulating H3Cit by enzyme-linked immunosorbent assay (ELISA), as well as bound to MVs quantified by flow cytometry. H3Cit-bearing MVs expressed neutrophil and/or platelet surface markers, indicating platelet-neutrophil interactions. In addition, in vitro experiments revealed that H3Cit can bind to phosphatidylserine exposed on platelet derived MVs. Taken together; our results demonstrate that NETs can be detected in peripheral blood during endotoxemia by two distinct H3Cit-specific methods. Furthermore, we propose a previously unrecognized mechanism by which H3Cit may be disseminated throughout the vasculature by the binding to MVs.
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  • Lasselin, Julie, et al. (författare)
  • Communication of health in experimentally sick men and women : A pilot study
  • 2018
  • Ingår i: Psychoneuroendocrinology. - : Elsevier BV. - 0306-4530 .- 1873-3360. ; 87, s. 188-195
  • Tidskriftsartikel (refereegranskat)abstract
    • The way people communicate their ill-health and the factors involved in ill-health communication remain poorly known. In the present study, we tested how men and women communicate their sickness and assessed whether sickness-related variables (i.e., body temperature, immune response, subjective sickness symptoms) predicted communicative behaviors. Twenty-two participants were filmed during experimentally induced sickness, triggered by lipopolysaccharide administration (2ng/kg body weight), and after placebo administration, in presence of female care providers. Two trained raters scored participants' communicative behaviors (verbal complaints, moaning and sighs/deep breaths). The physiological and subjective sickness responses were similar in both sexes. Participants were more likely to moan and complain when sick, although the frequency of these behaviors remained low and no clear sex differences was observed. Nevertheless, frequency of sighs/deep breaths was increased amongst sick men but not in women. Sickness-related variables did not predict sigh/deep breath frequency. In this setting, sick men appear to display a lower threshold of expressing their malaise as compared to similarly sick women.
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  • Lasselin, Julie, et al. (författare)
  • Sex differences in how inflammation affects behavior : What we can learn from experimental inflammatory models in humans
  • 2018
  • Ingår i: Frontiers in neuroendocrinology (Print). - : Elsevier BV. - 0091-3022 .- 1095-6808. ; 50, s. 91-106
  • Forskningsöversikt (refereegranskat)abstract
    • Human models demonstrate that experimental activation of the innate immune system has profound effects on brain activation and behavior, inducing fatigue, worsened mood and pain sensitivity. It has been proposed that inflammation is a mechanism involved in the etiology and maintenance of depression, chronic pain and long-term fatigue. These diseases show a strong female overrepresentation, suggesting that a better understanding of sex differences in how inflammation drives behavior could help the development of individualized treatment interventions. For this purpose, we here review sex differences in studies using experimental inflammatory models to investigate changes in brain activity and behavior. We suggest a model in which inflammation accentuates sex differences in brain networks and pre-existing vulnerability factors. This effect could render women more vulnerable to the detrimental effects of immune-to-brain communication over time. We call for systematic and large scale investigations of vulnerability factors for women in the behavioral response to inflammation.
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  • Lasselin, Julie, et al. (författare)
  • Sickness behavior is not all about the immune response : Possible roles of expectations and prediction errors in the worry of being sick
  • 2018
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 74, s. 213-221
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundPeople react very differently when sick, and there are only poor correlations between the intensity of the immune response and sickness behavior. Yet, alternative predictors of the individual differences in sickness are under-investigated. Based on the predictive coding model of placebo responses, where health outcomes are function of bottom-up sensory information and top-down expectancies, we hypothesized that individual differences in behavioral changes during sickness could be explained by individual top-down expectancies and prediction errors.MethodsTwenty-two healthy participants were made sick by intravenously administering lipopolysaccharide (2 ng/kg body weight). Their expectations of becoming sick were assessed before the injection.ResultsParticipants having lower expectations of becoming sick before the injection reacted with more emotional distress (i.e., more negative affect and lower emotional arousal) than those with high expectations of becoming sick, despite having similar overall sickness behavior (i.e., a combined factor including fatigue, pain, nausea and social withdrawal). In keeping with a predictive coding model, the “prediction error signal”, i.e., the discrepancy between the immune signal and sickness expectancy, predicted emotional distress (reduction in emotional arousal in particular).ConclusionThe current findings suggest that the emotional component of sickness behavior is, at least partly, shaped by top-down expectations. Helping patients having a realistic expectation of symptoms during treatment of an illness may thus reduce aggravated emotional responses, and ultimately improve patients’ quality of life and treatment compliance.Registration“Endotoxin-induced Inflammatory and Behavioral Responses and Predictors of Individual Differences”, https://clinicaltrials.gov/ct2/show/NCT02529592, registration number: NCT02529592.
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