Publications by authors named "Alan Chant"

Objective: Anonymised patient-level data from clinical research are increasingly recognised as a fundamental and valuable resource. It has value beyond the original research project and can help drive scientific research and innovations and improve patient care. To support responsible data sharing, we need to develop systems that work for all stakeholders.

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Background: Numerous frameworks for supporting, evaluating and reporting patient and public involvement in research exist. The literature is diverse and theoretically heterogeneous.

Objectives: To identify and synthesize published frameworks, consider whether and how these have been used, and apply design principles to improve usability.

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Background And Aims: Historically, patient and public involvement (PPI) in the design and conduct of surgical trials has been absent or minimal, but it is now routinely recommended and even required by some research funders. We aimed to identify and describe current PPI practice in surgical trials in the United Kingdom, and to explore the views and experiences of surgical trial staff and patient or public contributors in relation to these practices. This was part of a larger study to inform development of a robust PPI intervention aimed at improving recruitment and retention in surgical trials.

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Objective: To investigate the impact of patient and public involvement (PPI) on rates of enrolment and retention in clinical trials and explore how this varies with the context and nature of PPI.

Design: Systematic review and meta-analysis.

Data Sources: Ten electronic databases, including Medline, INVOLVE Evidence Library, and clinical trial registries.

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Introduction: Adherence to and persistence of medications for chronic diseases remains poor and many interventions to improve medication use have only been modestly effective. Targeting interventions to patients who are most likely to benefit should improve their efficiency and clinical impact. This study aims to test the impact of three cost-equivalent pharmacist-led interventions on insulin persistence and glycaemic control among patients with diabetes.

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Calmodulin from is an α-helical calcium-binding protein that expresses to high levels in . When the N-terminus of a calmodulin variant is bound to Ca, it undergoes a conformational change, exposing hydrophobic pockets. This property can be utilized for purification purposes, as these pockets bind to phenyl sepharose resin with high affinity.

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Article Synopsis
  • - The study investigates type I NKT cells, an important part of the immune response, and finds a notable lack of these cells in certain wild-derived inbred mouse strains like PWD/PhJ, SPRET/EiJ, and CAST/EiJ.
  • - It identifies that the PWD/PhJ strain has significantly reduced levels of CD1d gene and protein expression due to impaired promoter activity, which affects the ability of thymocytes and dendritic cells to present antigens to NKT cells.
  • - The researchers pinpoint two specific single nucleotide changes in the CD1d promoter that contribute to this reduced expression, highlighting genetic factors that may influence the presence of NKT cells in different mouse strains and potentially impacting the evolution of
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NKT cells are known to rapidly produce a large amount of cytokines upon activation. Although a number of signaling pathways that regulate the development of NKT cells have been identified, the signaling pathways involved in the regulation of NKT cell cytokine production remain unclear. In this study, we show that the p38 MAPK pathway is dispensable for the development of NKT cells.

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CD1d-restricted NKT cells make up an innate-like T cell subset that plays a role in amplifying the response of innate immune leukocytes to TLR ligands. The Slam locus contains genes that have been implicated in innate and adaptive immune responses. In this study, we demonstrate that divergent Slam locus haplotypes modulate the response of macrophages to the TLR4 ligand LPS through their control of NKT cell number and function.

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It is assumed that complement and noncomplement-mediated mechanisms are similarly responsible for Campath-1H-mediated killing of all T-cell subtypes in vivo. However, the differing surface expression of CD52 on T-cell subtypes suggests that may not be the case. The purpose of this study is to determine the extent and mechanism of Campath-1H-mediated elimination of different T-cell subtypes in peripheral blood.

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To successfully induce donor-specific tolerance after immune depletion, it is essential to understand the residual and recovering immune system in the context of the depleting agent because the properties of such a recovering immune system differ based on the depleting agent used. In this study, we investigate the phenotypic and functional characteristics of T cells exposed to Campath-1H in vivo and in vitro. Recovering T cells demonstrated down modulated surface CD4 and CD8 (by flow cytometry) for up to 45 days after Campath-1H administration.

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Histidine (His) tags are one of the most popular fusion tags for the isolation of proteins via metal affinity chromatography. The fusion tag is routinely left attached to the protein when carrying out experiments, with the assumption that the addition has no effect on structure or function. In the present study, we have prepared four proteins of the gene regulatory protein AreA from Aspergillus nidulans for crystallization experiments: a 91-amino acid peptide encompassing the minimal DNA-binding region, both with and without the His-tag (HZFB and ZFB, respectively), and a 155-amino acid protein previously proposed to be the entire DNA-binding domain for AreA, both with and without the His-tag (HG1b and G1b, respectively).

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The 876-aa protein AreA regulates the expression of numerous genes involved in nitrogen metabolism in Aspergillus nidulans, and interacts with GATA sequences upstream of the relevant genes. We have carried out limited proteolysis of the C-terminal domain of the AreA protein in order to identify possible structural domains within the protein. A stable 156-amino-acid fragment was identified that contained the zinc finger region, and this sequence was cloned and expressed in E.

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