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Kathleen N. Potter

Researcher at University of Southampton

Publications -  82
Citations -  4932

Kathleen N. Potter is an academic researcher from University of Southampton. The author has contributed to research in topics: Deprescribing & Chronic lymphocytic leukemia. The author has an hindex of 33, co-authored 72 publications receiving 4328 citations. Previous affiliations of Kathleen N. Potter include Oklahoma Medical Research Foundation & University of Western Australia.

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Reducing Inappropriate Polypharmacy: The Process of Deprescribing

TL;DR: A deprescribing protocol is proposed comprising 5 steps: ascertain all drugs the patient is currently taking and the reasons for each one, and prioritize drugs for discontinuation that have the lowest benefit-harm ratio and lowest likelihood of adverse withdrawal reactions or disease rebound syndromes.
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The feasibility and effect of deprescribing in older adults on mortality and health: a systematic review and meta-analysis

TL;DR: In this article, a review aimed to determine whether or not deprescribing is a safe, effective and feasible intervention to modify mortality and health outcomes in older adults, and the authors found that although non-randomized data suggested that deprecribing reduces mortality, depresncribing was not shown to alter mortality in randomized studies.
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Somatic Hypermutation Introduces Insertions and Deletions into Immunoglobulin V Genes

TL;DR: Five insertion and four deletion events in otherwise somatically mutated VH gene cDNA molecules are described, consistent with models of somatic hypermutation involving an unstable polymerase enzyme complex lacking proofreading capabilities, and suggest a downregulation or alteration of DNA repair at the V locus during the hypermutations process.
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Reversible anergy of sIgM-mediated signaling in the two subsets of CLL defined by VH-gene mutational status.

TL;DR: Stating that unmutated cases (U-CLL) have an increased ability to phosphorylate p72(Syk) in response to sIgM ligation compared to mutated cases (M-C LL), this is confirmed and further investigate this differential signaling in a large cohort by [Ca(2+)](i) mobilization.
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Fc gamma receptor IIb on target B cells promotes rituximab internalization and reduces clinical efficacy

TL;DR: Target-cell FcγRIIb provides a potential biomarker of response to type I anti-CD20 mAb and promotes internalization of rituximab in a dose-dependent manner and is largely responsible for the observed heterogeneity across a range of B-cell malignancies.