Publications by authors named "J R Platt"

Contrails, formed by aircraft engines, are a major component of aviation's impact on anthropogenic climate change. Contrail avoidance is a potential option to mitigate this warming effect, however, uncertainties surrounding operational constraints and accurate formation prediction make it unclear whether it is feasible. Here we address this gap with a feasibility test through a randomized controlled trial of contrail avoidance in commercial aviation at the per-flight level.

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Immune surveillance depends in part on the recognition of peptide variants by T cell antigen receptors. Given that both normal B cells and malignant B cells accumulate mutations we chose a murine model of multiple myeloma to test conditions to induce cell-mediated immunity targeting malignant plasma cell (PC) clones but sparing of normal PCs. Revealing a previously unknown function for intracellular C3d, we found that C3d engaged T cell responses against malignant PC in the bone marrow of mice that had developed multiple myeloma spontaneously.

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Article Synopsis
  • The audit aimed to assess and improve the completeness and accuracy of the National Joint Registry (NJR) dataset specifically for elbow arthroplasty surgeries.
  • In a two-phase approach, Phase 1 compared NJR data with NHS England Hospital Episode Statistics (HES), identifying thousands of unmatched and inaccurate records, particularly for radial head arthroplasties (RHAs).
  • Phase 2 involved collaboration among 142 NHS hospitals to correct and update records, resulting in an improved completeness of the NJR dataset from 63% to 93% and accuracy from 94% to 98%.
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The pathogenic mechanisms of many diseases are well understood at the molecular level, but there are prevalent syndromes associated with pathogenic signaling, such as diabetes and chronic inflammation, where our understanding is more limited. Here, we report that pathogenic signaling suppresses the mobility of a spectrum of proteins that play essential roles in cellular functions known to be dysregulated in these chronic diseases. The reduced protein mobility, which we call proteolethargy, was linked to cysteine residues in the affected proteins and signaling-related increases in excess reactive oxygen species.

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