Seeing Is Believing: Extravascular Platelet Recruitment in Asthma and Allergic Inflammation.
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ABSTRACT:
SUBMITTER: Johansson MW
PROVIDER: S-EPMC8086035 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Knowledge of factors that trigger human response to climate change is crucial for effective climate change policy communication. Climate change has been claimed to have low salience as a risk issue because it cannot be directly experienced. Still, personal factors such as strength of belief in local effects of climate change have been shown to correlate strongly with responses to climate change and there is a growing literature on the hypothesis that personal experience of climate change (and/or its effects) explains responses to climate change. Here we provide, using survey data from 845 private forest owners operating in a wide range of bio-climatic as well as economic-social-political structures in a latitudinal gradient across Europe, the first evidence that the personal strength of belief and perception of local effects of climate change, highly significantly explain human responses to climate change. A logistic regression model was fitted to the two variables, estimating expected probabilities ranging from 0.07 (SD ± 0.01) to 0.81 (SD ± 0.03) for self-reported adaptive measures taken. Adding socio-demographic variables improved the fit, estimating expected probabilities ranging from 0.022 (SD ± 0.008) to 0.91 (SD ± 0.02). We conclude that to explain and predict adaptation to climate change, the combination of personal experience and belief must be considered.
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Project description:BackgroundSkin and soft-tissue infections are very common among persons who inject drugs. They occur when microbes pass under the protective layer of the skin and proliferate. This happens when harm reduction recommendations such as skin aseptia before injection and sterile injection equipment usage are not properly followed.MethodsA group of active drug users involved in a health promotion project as peer educators were asked about their formation needs. To address their inquiries concerning skin and soft-tissue infections, we devised with them a series of workshops touching upon common infections, the microflora, and microbial transmission.ResultsParticipants learned to identify common infections and how to properly react in case of an abscess, cellulitis or phlebitis. They saw microscopic objects, found out about the high prevalence of microbes in their environment and on their skin, and could appreciate the efficiency of different washing and disinfection techniques. They visualized how easily microbes can spread from person to person and from contaminated objects to persons.ConclusionIn the weeks following this activity, some participants demonstrated and reported healthy behavioural changes regarding their own injection practices. Furthermore, they shared their newfound knowledge and began enforcing its application among people they inject drugs with. Most participants greatly appreciated this activity and valued it as being highly efficient and tangible. Note: A French version of this paper is available on the Journal's web site [see Additional file 1].
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Project description: Not available
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Project description:Determination of ground-state spins of open-shell transition-metal complexes is critical to understanding catalytic and materials properties but also challenging with approximate electronic structure methods. As an alternative approach, we demonstrate how structure alone can be used to guide assignment of ground-state spin from experimentally determined crystal structures of transition-metal complexes. We first identify the limits of distance-based heuristics from distributions of metal-ligand bond lengths of over 2000 unique mononuclear Fe(II)/Fe(III) transition-metal complexes. To overcome these limits, we employ artificial neural networks (ANNs) to predict spin-state-dependent metal-ligand bond lengths and classify experimental ground-state spins based on agreement of experimental structures with the ANN predictions. Although the ANN is trained on hybrid density functional theory data, we exploit the method-insensitivity of geometric properties to enable assignment of ground states for the majority (ca. 80-90%) of structures. We demonstrate the utility of the ANN by data-mining the literature for spin-crossover (SCO) complexes, which have experimentally observed temperature-dependent geometric structure changes, by correctly assigning almost all (>95%) spin states in the 46 Fe(II) SCO complex set. This approach represents a promising complement to more conventional energy-based spin-state assignment from electronic structure theory at the low cost of a machine learning model.
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Project description:1. Although anti-alpha(4) integrin mAbs reduce eosinophil accumulation in several models of allergic inflammation, it is not clear whether this occurs via a direct action to block eosinophil alpha(4) integrins or indirectly on another cell type. The role of alpha(4) integrins on the accumulation of (111)In-labelled eosinophils in allergic and non-allergic inflammation in guinea-pig skin was therefore investigated. 2. Intradermal injection of antigen in sensitized skin sites induced accumulation of (111)In-eosinophils that was reduced up to 70% by two anti-alpha(4) integrin mAbs. In contrast, accumulation of (111)In-eosinophils to intradermal chemoattractants was unaffected by the same mAbs. 3. Accumulation of (111)In-eosinophils in allergic and non-allergic conditions was partly inhibited by a low dose of an anti-beta(2) integrin mAb. In combination with anti-alpha(4) integrin mAb, responses were not further reduced suggesting that these adhesion pathways are not additive or synergic. 4. Pretreating skin sites with antiserum or contaminating LPS did not reveal an alpha(4) integrin dependent pathway for chemoattractant-induced (111)In-eosinophil accumulation. These data suggest that alpha(4) integrins are involved in the response to antigen in sensitized skin sites. 5. Pretreating (111)In-eosinophil with alpha(4) integrin mAb blocked their adhesion to fibronectin in vitro but did not inhibit their accumulation in allergic inflammation suggesting that the blocking effect in vivo was eosinophil independent. 6. These data support the concept that targeting alpha(4) integrins on cells other than eosinophils could control eosinophil accumulation and have therapeutic potential in allergic diseases such as asthma and atopic dermatitis.
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Project description:Allergic asthma is characterized by airway eosinophilia, increased mucin production and allergen-specific IgE. Fc gamma receptor IIb (FcgammaRIIb), an inhibitory IgG receptor, has recently emerged as a negative regulator of allergic diseases like anaphylaxis and allergic rhinitis. However, no studies to date have evaluated its role in allergic asthma. Our main objective was to study the role of FcgammaRIIb in allergic lung inflammation. We used a murine model of allergic airway inflammation. Inflammation was quantified by BAL inflammatory cells and airway mucin production. FcgammaRIIb expression was measured by qPCR and flow cytometry and the cytokines were quantified by ELISA. Compared to wild type animals, FcgammaRIIb deficient mice mount a vigorous allergic lung inflammation characterized by increased bronchoalveolar lavage fluid cellularity, eosinophilia and mucin content upon ragweed extract (RWE) challenge. RWE challenge in sensitized mice upregulated FcgammaRIIb in the lungs. Disruption of IFN-gamma gene abrogated this upregulation. Treatment of naïve mice with the Th1-inducing agent CpG DNA increased FcgammaRIIb expression in the lungs. Furthermore, treatment of sensitized mice with CpG DNA prior to RWE challenge induced greater upregulation of FcgammaRIIb than RWE challenge alone. These observations indicated that RWE challenge upregulated FcgammaRIIb in the lungs by IFN-gamma- and Th1-dependent mechanisms. RWE challenge upregulated FcgammaRIIb on pulmonary CD14+/MHC II+ mononuclear cells and CD11c+ cells. FcgammaRIIb deficient mice also exhibited an exaggerated RWE-specific IgE response upon sensitization when compared to wild type mice. We propose that FcgammaRIIb physiologically regulates allergic airway inflammation by two mechanisms: 1) allergen challenge mediates upregulation of FcgammaRIIb on pulmonary CD14+/MHC II+ mononuclear cells and CD11c+ cells by an IFN-gamma dependent mechanism; and 2) by attenuating the allergen specific IgE response during sensitization. Thus, stimulating FcgammaRIIb may be a therapeutic strategy in allergic airway disorders.
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