90 research outputs found

    Identity and typification of Achroomyces effusus (Pucciniomycotina, Basidiomycota)

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    The identity of Achroomyces effusus is re-established with the use of morphological and DNA methods, and a neotype is selected. The species is conspecific with Colacogloea peniophorae, the generic type of Colacogloea, and has a priority over it. A new combination, C. effusa, is proposed.Peer reviewe

    Genetic identification of cell types underlying brain complex traits yields insights into the etiology of Parkinson's disease

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    Genome-wide association studies have discovered hundreds of loci associated with complex brain disorders, but it remains unclear in which cell types these loci are active. Here we integrate genome-wide association study results with single-cell transcriptomic data from the entire mouse nervous system to systematically identify cell types underlying brain complex traits. We show that psychiatric disorders are predominantly associated with projecting excitatory and inhibitory neurons. Neurological diseases were associated with different cell types, which is consistent with other lines of evidence. Notably, Parkinson's disease was genetically associated not only with cholinergic and monoaminergic neurons (which include dopaminergic neurons) but also with enteric neurons and oligodendrocytes. Using post-mortem brain transcriptomic data, we confirmed alterations in these cells, even at the earliest stages of disease progression. Our study provides an important framework for understanding the cellular basis of complex brain maladies, and reveals an unexpected role of oligodendrocytes in Parkinson's disease

    Genetic identification of cell types underlying brain complex traits yields insights into the etiology of Parkinson's disease

    Get PDF
    Genome-wide association studies have discovered hundreds of loci associated with complex brain disorders, but it remains unclear in which cell types these loci are active. Here we integrate genome-wide association study results with single-cell transcriptomic data from the entire mouse nervous system to systematically identify cell types underlying brain complex traits. We show that psychiatric disorders are predominantly associated with projecting excitatory and inhibitory neurons. Neurological diseases were associated with different cell types, which is consistent with other lines of evidence. Notably, Parkinson’s disease was genetically associated not only with cholinergic and monoaminergic neurons (which include dopaminergic neurons) but also with enteric neurons and oligodendrocytes. Using post-mortem brain transcriptomic data, we confirmed alterations in these cells, even at the earliest stages of disease progression. Our study provides an important framework for understanding the cellular basis of complex brain maladies, and reveals an unexpected role of oligodendrocytes in Parkinson’s disease.</p

    Modelling the two-way coupling of tidal sand waves and benthic organisms:a linear stability approach

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    We use a linear stability approach to develop a process-based morphodynamic model including a two-way coupling between tidal sand wave dynamics and benthic organisms. With this model we are able to study both the effect of benthic organisms on the hydro- and sediment dynamics, and the effect of spatial and temporal environmental variations on the distribution of these organisms. Specifically, we include two coupling processes: the effect of the biomass of the organisms on the bottom slip parameter, and the effect of shear stress variations on the biological carrying capacity. We discuss the differences and similarities between the methodology used in this work and that from ‘traditional’ (morphodynamics only) stability modelling studies. Here, we end up with a 2×2 linear eigenvalue problem, which leads to two distinct eigenmodes for each topographic wave number. These eigenmodes control the growth and migration properties of both sand waves and benthic organisms (biomass). Apart from hydrodynamic forcing, the biomass also grows autonomously, which results in a changing fastest growing mode (FGM, i.e. the preferred wavelength) over time. As a result, in contrast to ‘traditional’ stability modelling studies, the FGM for a certain model outcome does not necessarily have to be dominant in the field. Therefore, we also analysed the temporal evolution of an initial bed hump (without perturbing biomass) and of an initial biomass hump (without perturbing topography). It turns out that these local disturbances may trigger the combined growth of sand waves and spatially varying biomass patterns. Moreover, the results reveal that the autonomous benthic growth significantly influences the growth rate of sand waves. Finally, we show that biomass maxima tend to concentrate in the region around the trough and lee side slope of sand waves, which corresponds to observations in the field

    Effector mechanisms of interleukin-17 in collagen-induced arthritis in the absence of interferon-γ and counteraction by interferon-γ

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    Introduction Interleukin (IL)-17 is a pro-inflammatory cytokine in rheumatoid arthritis (RA) and collagen-induced arthritis ( CIA). Since interferon (IFN)-gamma inhibits Th17 cell development, IFN-gamma receptor knockout (IFN-gamma R KO) mice develop CIA more readily. We took advantage of this model to analyse the mechanisms of action of IL-17 in arthritis. The role of IFN-gamma on the effector mechanisms of IL-17 in an in vitro system was also investigated. Methods IFN-gamma R KO mice induced for CIA were treated with anti-IL-17 or control antibody. The collagen type II (CII)-specific humoral and cellular autoimmune responses, myelopoiesis, osteoclastogenesis, and systemic cytokine production were determined. Mouse embryo fibroblasts (MEF) were stimulated with IL-17, tumor necrosis factor (TNF)-alpha and the expression of cytokines and chemokines were determined. Results A preventive anti-IL-17 antibody treatment inhibited CIA in IFN gamma R KO mice. In the joints of anti-IL-17-treated mice, neutrophil influx and bone destruction were absent. Treatment reduced the cellular autoimmune response as well as the splenic expansion of CD11b(+) cells, and production of myelopoietic cytokines such as granulocyte macrophage colony-stimulating factor (GM-CSF) and IL-6. IL-17 and TNF-alpha synergistically induced granulocyte chemotactic protein-2 (GCP-2), IL-6 and receptor activator of NF kappa B ligand (RANKL) in MEF. This induction was profoundly inhibited by IFN-gamma in a STAT-1 (signal transducer and activator of transcription-1)dependent way. Conclusions In the absence of IFN-gamma, IL-17 mediates its proinflammatory effects mainly through stimulatory effects on granulopoiesis, neutrophil infiltration and bone destruction. In vitro IFN-gamma profoundly inhibits the effector function of IL-17. Thus, aside from the well-known inhibition of the development of Th17 cells by IFN-gamma, this may be an additional mechanism through which IFN-gamma attenuates autoimmune diseases

    Modelling social identification and helping in evacuation simulation

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    Social scientists have criticised computer models of pedestrian streams for their treatment of psychological crowds as mere aggregations of individuals. Indeed most models for evacuation dynamics use analogies from physics where pedestrians are considered as particles. Although this ensures that the results of the simulation match important physical phenomena, such as the deceleration of the crowd with increasing density, social phenomena such as group processes are ignored. In particular, people in a crowd have social identities and share those social identities with the others in the crowd. The process of self categorisation determines norms within the crowd and influences how people will behave in evacuation situations. We formulate the application of social identity in pedestrian simulation algorithmically. The goal is to examine whether it is possible to carry over the psychological model to computer models of pedestrian motion so that simulation results correspond to observations from crowd psychology. That is, we quantify and formalise empirical research on and verbal descriptions of the effect of group identity on behaviour. We use uncertainty quantification to analyse the model’s behaviour when we vary crucial model parameters. In this first approach we restrict ourselves to a specific scenario that was thoroughly investigated by crowd psychologists and where some quantitative data is available: the bombing and subsequent evacuation of a London underground tube carriage on July 7th 2005

    Plasticity of lifelong calorie-restricted C57BL/6J mice in adapting to a medium-fat diet intervention at old age

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    Calorie restriction (CR) is a dietary regimen that supports healthy aging. In this study we investigated the systemic and liver-specific responses caused by a diet switch to a medium-fat (MF) diet in 24-month-old life-long, CR-exposed mice. This study aimed to increase the knowledge base on dietary alterations of gerontological relevance. Nine-week-old C57BL/6J mice were exposed either to a control, CR or MF diet. At the age of 24 months, a subset of mice of the CR group was transferred to ad libitum MF feeding (CR-MF). The mice were sacrificed at the age of 28 months, then biochemical and molecular analyses were performed. Our results showed that, despite the long-term exposure to the CR regimen, mice in the CR-MF group displayed hyperphagia, rapid weight gain, and hepatic steatosis. However, no hepatic fibrosis/injury or alteration in CR-improved survival was observed in the diet switch group. The liver transcriptomic profile of CR-MF mice largely shifted to a profile similar to the MF-fed animals but leaving ~22% of the 1578 differentially regulated genes between the CR and MF diet groups comparable with the expression of the life-long CR group. Therefore, although the diet switch was performed at an old age, the CR-MF-exposed mice showed plasticity in coping with the challenge of a MF diet without developing severe liver pathologies

    The implications of the COVID-19 pandemic on eating disorder features and comorbid psychopathology among adolescents with anorexia nervosa and matched controls:a comparative cohort design study

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    PurposeTo examine implications of the COVID-19 pandemic on eating disorder (ED) features and psychopathology in female adolescents with anorexia nervosa (AN).MethodIn total 79 females with first-onset AN (aged 12-22 years) were included and were followed up across a period of 1 year. We assessed AN participants recruited pre-pandemic (n = 49) to those recruited peri-pandemic (n = 30). Pre- (n = 37) and peri-pandemic (n = 38) age-, and education-matched typically developing (TD) girls (n = 75) were used as a reference cohort. ED features and psychopathology were assessed at baseline. After 1 year of follow-up the association between pandemic timing and clinical course was assessed. Analyses of covariance were used to examine differences in ED features and psychopathology.ResultsPeri-pandemic AN participants experienced less ED symptoms at baseline compared to pre-pandemic AN participants. In particular, they were less dissatisfied with their body shape, and experienced less interpersonal insecurity. In addition, the peri-pandemic AN group met fewer DSM-IV criteria for comorbid disorders, especially anxiety disorders. In contrast, peri-pandemic AN participants had a smaller BMI increase over time. In TD girls, there were no differences at baseline in ED features and psychopathology between the pre- and peri-pandemic group.ConclusionOverall, peri-pandemic AN participants were less severely ill, compared to pre-pandemic AN participants, which may be explained by less social pressure and peer contact, and a more protective parenting style during the pandemic. Conversely, peri-pandemic AN participants had a less favorable clinical course, which may be explained by reduced access to health care facilities during the pandemic.Level of evidenceLevel III: Evidence obtained from well-designed cohort or case-control analytic studies
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