18 research outputs found

    How does it really feel to act together? : Shared emotions and the phenomenology of we-agency

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    Research on the phenomenology of agency for joint action has so far focused on the sense of agency and control in joint action, leaving aside questions on how it feels to act together. This paper tries to fill this gap in a way consistent with the existing theories of joint action and shared emotion. We first reconstruct Pacherie’s (Phenomenology and the Cognitive Sciences, 13, 25–46, 2014) account on the phenomenology of agency for joint action, pointing out its two problems, namely (1) the necessary trade-off between the sense of self- and we-agency; and (2) the lack of affective phenomenology of joint action in general. After elaborating on these criticisms based on our theory of shared emotion, we substantiate the second criticism by discussing different mechanisms of shared affect—feelings and emotions—that are present in typical joint actions. We show that our account improves on Pacherie’s, first by introducing our agentive model of we-agency to overcome her unnecessary dichotomy between a sense of self- and we-agency, and then by suggesting that the mechanisms of shared affect enhance not only the predictability of other agents’ actions as Pacherie highlights, but also an agentive sense of we-agency that emerges from shared emotions experienced in the course and consequence of joint action.Peer reviewe

    Unity in defence: honeybee workers exhibit conserved molecular responses to diverse pathogens

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    This is the final version of the article. Available from the publisher via the DOI in this record.Background: Organisms typically face infection by diverse pathogens, and hosts are thought to have developed specific responses to each type of pathogen they encounter. The advent of transcriptomics now makes it possible to test this hypothesis and compare host gene expression responses to multiple pathogens at a genome-wide scale. Here, we performed a meta-analysis of multiple published and new transcriptomes using a newly developed bioinformatics approach that filters genes based on their expression profile across datasets. Thereby, we identified common and unique molecular responses of a model host species, the honey bee (Apis mellifera), to its major pathogens and parasites: the Microsporidia Nosema apis and Nosema ceranae, RNA viruses, and the ectoparasitic mite Varroa destructor, which transmits viruses. Results: We identified a common suite of genes and conserved molecular pathways that respond to all investigated pathogens, a result that suggests a commonality in response mechanisms to diverse pathogens. We found that genes differentially expressed after infection exhibit a higher evolutionary rate than non-differentially expressed genes. Using our new bioinformatics approach, we unveiled additional pathogen-specific responses of honey bees; we found that apoptosis appeared to be an important response following microsporidian infection, while genes from the immune signalling pathways, Toll and Imd, were differentially expressed after Varroa/virus infection. Finally, we applied our bioinformatics approach and generated a gene co-expression network to identify highly connected (hub) genes that may represent important mediators and regulators of anti-pathogen responses. Conclusions: Our meta-analysis generated a comprehensive overview of the host metabolic and other biological processes that mediate interactions between insects and their pathogens. We identified key host genes and pathways that respond to phylogenetically diverse pathogens, representing an important source for future functional studies as well as offering new routes to identify or generate pathogen resilient honey bee stocks. The statistical and bioinformatics approaches that were developed for this study are broadly applicable to synthesize information across transcriptomic datasets. These approaches will likely have utility in addressing a variety of biological questions.This article is a joint effort of the working group TRANSBEE and an outcome of two workshops kindly supported by sDiv, the Synthesis Centre for Biodiversity Sciences within the German Centre for Integrative Biodiversity Research (iDiv) Halle-Jena-Leipzig, funded by the German Science Foundation (FZT 118). New datasets were performed thanks to the Insect Pollinators Initiative (IPI grant BB/I000100/1 and BB/I000151/1), with participation of the UK-USA exchange funded by the BBSRC BB/I025220/1 (datasets #4, 11 and 14). The IPI is funded jointly by the Biotechnology and Biological Sciences Research Council, the Department for Environment, Food and Rural Affairs, the Natural Environment Research Council, the Scottish Government and the Wellcome Trust, under the Living with Environmental Change Partnershi

    Susceptibility-weighted imaging in stroke-like migraine attacks after radiation therapy syndrome

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    Stroke-like migraine attacks after radiation therapy (SMART) syndrome has a characteristic clinical presentation and postcontrast T1WI MRI appearance. Susceptibility-weighted imaging (SWI) may help distinguish SMART from other disorders that may have a similar postcontrast MRI appearance. The MRI examinations of four patients with SMART syndrome are described herein, each of which included SWI, FLAIR, DWI, and postcontrast T1WI on the presenting and follow-up MRI examinations. In each, the initial SWI MRI demonstrated numerous susceptibility hypointensities < 5 mm in size throughout the cerebrum, particularly within the periventricular white matter (PVWM), presumably related to radiation-induced cavernous hemangiomas (RICHs). By follow-up MRI, each postcontrast examination had demonstrated resolution of the gyriform enhancement on T1WI, without susceptibility hypointensities on SWI within those previously enhancing regions. These preliminary findings suggest that SWI may help identify SMART syndrome or at least help discriminate it from other disorders, by the findings of numerous susceptibility hypointensities on SWI likely representing RICHs, gyriform enhancement on T1WI, and postsurgical findings or appropriate clinical history

    All that bleeds is not black: susceptibility weighted imaging of intracranial hemorrhage and the effect of T1 signal

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    To determine if intracranial hemorrhages (ICH) are always hypointense on Susceptibility weighted imaging (SWI) and to determine the effect of T1-signal intensity on the appearance of ICH in SWI series. SWI and T1-signal intensities of ICH were retrospectively studied in a series of patients. SWI signal intensities were statistically correlated with T1-signal intensities. In a series of 57 MRI scans from 40 patients, ICH was hypointense in 19, mixed-intensity in 21, and hyperintense in 17. Hyperintensity of ICH on SWI was significantly associated with increased T1 signal (P<.001). ICH can have a varied appearance on SWI

    Childhood Cerebral Adrenoleukodystrophy: MR Perfusion Measurements and their Use in Predicting Clinical Outcome after Hematopoietic Stem Cell Transplantation

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    BACKGROUND AND PURPOSE: To prospectively measure MR perfusion (MRP) parameters in patients with cerebral adrenoleukodystrophy (cALD) pre- and post-hematopoietic stem cell transplantation (HSCT), and to correlate those measurements with the clinical outcome. MATERIALS AND METHODS: Ten cALD patients prospectively underwent DSC-MRP at <45 days pre-(baseline), 30–60 days post-, and 1 year post-HSCT. MRP measurements in the 10 patients and 8 controls were obtained from the parietooccipital WM (POWM), callosal splenium (SCC), leading enhancing edge (LEE), and normal-appearing frontal white matter (NAFWM). MR severity (Loes) scores and clinical neurologic function (NFS) and neurocognitive scores were also obtained. MRP values were analyzed in the cALD patients at each time point, and compared to controls. Correlations were calculated between the pre-HSCT MRP values and 1-year clinical scores, with p-value adjustment for multiple comparisons. RESULTS: At baseline in cALD patients, both rCBV and rCBF within the SCC and POWM significantly differed from controls (p=0.005–0.031), and remained so 1 year post-HSCT (p=0.003–0.005). Meanwhile, no MRP parameter within the LEE differed significantly from controls at baseline or at 1 year (p=0.074–0.999), nor significantly changed by 1 year post-HSCT (p=0.142–0.887). Baseline Loes scores correlated with 1 year NFS (r=0.813, p<0.0001), while SCC rCBV also significantly correlated with 1 year NFS, as well as the neurocognitive FSIQ and PIQ scores (r=−0.730–0.815, p=0.007–0.038). CONCLUSION: LEE measurements likely remain normal post-HSCT in cALD, suggesting local disease stabilization. Meanwhile, POWM and SCC rCBV and rCBF values worsen, signifying irreversible injury. Baseline SCC rCBV may predict clinical outcomes following HSCT
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