Effects of ultrafine particles on the allergic inflammation in the lung of asthmatics : results of a double-blinded randomized cross-over clinical pilot study

Background: Epidemiological and experimental studies suggest that exposure to ultrafine particles (UFP) might aggravate the allergic inflammation of the lung in asthmatics. Methods: We exposed 12 allergic asthmatics in two subgroups in a double-blinded randomized cross-over design, first to freshly generated ultrafine carbon particles (64 μg/m3; 6.1 ± 0.4 × 105 particles/cm3 for 2 h) and then to filtered air or vice versa with a 28-day recovery period in-between. Eighteen hours after each exposure, grass pollen was instilled into a lung lobe via bronchoscopy. Another 24 hours later, inflammatory cells were collected by means of bronchoalveolar lavage (BAL). (Trial registration: NCT00527462) Results: For the entire study group, inhalation of UFP by itself had no significant effect on the allergen induced inflammatory response measured with total cell count as compared to exposure with filtered air (p = 0.188). However, the subgroup of subjects, which inhaled UFP during the first exposure, exhibited a significant increase in total BAL cells (p = 0.021), eosinophils (p = 0.031) and monocytes (p = 0.013) after filtered air exposure and subsequent allergen challenge 28 days later. Additionally, the potential of BAL cells to generate oxidant radicals was significantly elevated at that time point. The subgroup that was exposed first to filtered air and 28 days later to UFP did not reveal differences between sessions. Conclusions: Our data demonstrate that pre-allergen exposure to UFP had no acute effect on the allergic inflammation. However, the subgroup analysis lead to the speculation that inhaled UFP particles might have a long-term effect on the inflammatory course in asthmatic patients. This should be reconfirmed in further studies with an appropriate study design and sufficient number of subjects

Semi-Metric Topology of the Human Connectome: Sensitivity and Specificity to Autism and Major Depressive Disorder

This is the final version of the article. It first appeared from PLOS via http://dx.doi.org/10.1371/journal.pone.0136388Introduction:\ud The human functional connectome is a graphical representation, consisting of nodes connected by edges, of the inter-relationships of blood oxygenation-level dependent (BOLD) time-series measured by MRI from regions encompassing the cerebral cortices and, often, the cerebellum. Semi-metric analysis of the weighted, undirected connectome distinguishes an edge as either direct (metric), such that there is no alternative path that is accumulatively stronger, or indirect (semi-metric), where one or more alternative paths exist that have greater strength than the direct edge. The sensitivity and specificity of this method of analysis is illustrated by two case-control analyses with independent, matched groups of adolescents with autism spectrum conditions (ASC) and major depressive disorder (MDD). \ud \ud Results:\ud Significance differences in the global percentage of semi-metric edges was observed in both groups, with increases in ASC and decreases in MDD relative to controls. Furthermore, MDD was associated with regional differences in left frontal and temporal lobes, the right limbic system and cerebellum. In contrast, ASC had a broadly increased percentage of semi-metric edges with a more generalised distribution of effects and some areas of reduction. In summary, MDD was characterised by localised, large reductions in the percentage of semi-metric edges, whilst ASC is characterised by more generalised, subtle increases. These differences were corroborated in greater detail by inspection of the semi-metric backbone for each group; that is, the sub-graph of semi-metric edges present in >90% of participants, and by nodal degree differences in the semi-metric connectome. \ud \ud Conclusion:\ud These encouraging results in what we believe is the first application of semi-metric analysis to neuroimaging data, raises confidence in the methodology as potentially capable of detection and characterisation of a range of neurodevelopmental and psychiatric disorders.This study was funded by the UK Medial Research Council (grants: G0802226 and G0701919), the National Institute for Health Research (NIHR) (grant: 06/05/01) and the Behavioural and Clinical Neuroscience Institute (BCNI), University of Cambridge. The BCNI is jointly funded by the Medical Research Council and the Wellcome Trust. Additional support was received from the NIHR Cambridge Biomedical Research Centre. CCH is supported by a Parke Davis Fellowship from the University of Cambridge and resides at Columbia University

Research data supporting "Semi-Metric Topology of the Human Connectome"

There are two sheets in the Excel spreadsheet. The first is the demographic data (age and gender) for the sample included in the study. The second sheet contains the semi-metric percentages derived from resting state functional MRI for each individual extracted from regions of interest of the cortex and cerebellum.This work was supported by the MRC [grant numbers MRC G0802226 and MRC G0701919], the NIHR, the Wellcome Trust and Parke-Davis

Measurement of the branching fraction and CPCP asymmetry in B+→J/ψρ+B^{+}\rightarrow J/\psi \rho^{+} decays

International audienceThe branching fraction and direct $C\!P$ asymmetry of the decay ${{{B} ^+}} \!\rightarrow {{J /\psi }} {{\rho } ^+}$ are measured using proton-proton collision data collected with the LHCb detector at centre-of-mass energies of 7 and 8 TeV, corresponding to a total integrated luminosity of 3 $\,\text{ fb }^{-1}$ . The following results are obtained: $\begin{aligned} \mathcal {B}({{B} ^+} \!\rightarrow {{J /\psi }} {{\rho } ^+} )&= (3.81^{+0.25-0.24} \pm 0.35) \times 10^{-5},\\ \mathcal {A}^{{C\!P}} ({{B} ^+} \!\rightarrow {{J /\psi }} {{\rho } ^+} )&= -0.045^{+0.056-0.057} \pm 0.008, \end{aligned}$ where the first uncertainties are statistical and the second systematic. Both measurements are the most precise to date