Publications by authors named "A H Marshall"

Background: Smoking rates in the UK have declined steadily over the past decades, masking considerable inequalities, as little change has been observed among people with a mental health condition. This trial sought to assess the feasibility and acceptability of supplying an electronic cigarette (e-cigarette) starter kit for smoking cessation as an adjunct to usual care for smoking cessation, to smokers with a mental health condition treated in the community, to inform a future effectiveness trial.

Methods: This randomised controlled feasibility trial, conducted March-December 2022, compared the intervention (e-cigarette starter kit with a corresponding information leaflet and demonstration with Very Brief Advice) with a 'usual care' control at 1-month follow-up.

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Pyramidal cells (PCs) in CA1 hippocampus can be classified by their radial position as deep or superficial and organize into subtype-specific circuits necessary for differential information processing. Specifically, superficial PCs receive fewer inhibitory synapses from parvalbumin (PV)-expressing interneurons than deep PCs, resulting in weaker feedforward inhibition of input from CA3 Schaffer collaterals. Using mice, we investigated mechanisms underlying CA1 PC differentiation and the development of this inhibitory circuit motif.

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A search for violation of the charge-parity (CP) symmetry in the D^{+}→K^{-}K^{+}π^{+} decay is presented, with proton-proton collision data corresponding to an integrated luminosity of 5.4  fb^{-1}, collected at a center-of-mass energy of 13 TeV with the LHCb detector. A novel model-independent technique is used to compare the D^{+} and D^{-} phase-space distributions, with instrumental asymmetries subtracted using the D_{s}^{+}→K^{-}K^{+}π^{+} decay as a control channel.

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Background: APOE4 carriers exhibit cerebrovascular dysfunction which may contribute to the development of cognitive decline and dementia; however, the mechanisms underlying this pathophysiology remain unknown. Impaired cerebrovascular reactivity (CVR) may be associated with vascular injury, inflammation, and endothelial dysfunction. To examine whether these processes may be involved in CVR deficits in APOE4 carriers, we explored whether plasma levels of vascular injury markers indicative of inflammation and endothelial dysfunction are associated with impaired CVR to hypercapnia and hypocapnia in older APOE4 carriers.

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