Mark Turner

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Andrej Dujella

University of Zagreb

Hemin Koyi

Uppsala University

Jana Javornik

University of East London

Graham Martin

University of Leicester

Gwen Robbins Schug

University of North Carolina at Greensboro

Gabriel Gutierrez-Alonso

University of Salamanca

John Sutton

Macquarie University

Eros Carvalho

Universidade Federal do Rio Grande do Sul

Kevin Arbuckle

Swansea University

Jesper Hoffmeyer

University of Copenhagen

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Papers by Mark Turner

Development of the Liverpool Adverse Drug Reaction Avoidability Assessment Tool

PloS one, 2017

To develop and test a new tool to assess the avoidability of adverse drug reactions that is suita... more To develop and test a new tool to assess the avoidability of adverse drug reactions that is suitable for use in paediatrics but which is also applicable to a variety of other settings. The study involved multiple phases. Preliminary work involved using the Hallas scale and a modification of the existing Hallas scale, to assess two different sets of adverse drug reaction (ADR) case reports. Phase 1 defined, modified and refined a new tool using multidisciplinary teams. Phase 2 involved the assessment of 50 ADR case reports from a prospective study of paediatric inpatients by individual assessors. Phase 3 compared assessments with the new tool for individuals and groups in comparison to the 'gold standard' (the avoidability outcome set by a panel of senior investigators: an experienced clinical pharmacologist, paediatrician and pharmacist). Inter-rater reliability (IRR), measure of disagreement and utilization of avoidability categories. Preliminary work-Pilot phase: results f...

Paediatric Adverse Drug Reactions (Adrs): A Comparison of a Newly Developed Avoidability Tool to Existing Hallas Assessments

Archives of disease in childhood, 2016

To compare a newly developed avoidability assessment tool (AAT) to existing Hallas assessments1 f... more To compare a newly developed avoidability assessment tool (AAT) to existing Hallas assessments1 for a set of paediatric ADR cases. The new AAT was employed to assess 249 case reports of ADRs causing admission to hospital. The case reports contained a description of the ADR, details of suspected and concurrent medication and past medical history. Each case report was independently assessed and an avoidability category assigned. For ADRs categorised as either 'possibly' or 'definitely avoidable' a rationale was recorded. A second reviewer independently assessed a purposive sample (10%) for validation and quality assurance purposes.The final outcome was then compared to the Hallas assessments (1) previously completed as part of another study, which was carried out in a consensus group setting. Both tools used categorical scores with the same four point ordinal scale 'definitely avoidable', 'possibly avoidable', 'not avoidable' and 'unassessab...

Phosphorylation of Excitation-Contraction Coupling Components in a Guinea-Pig Model of Heart Failure

Biophys J, 2010

extent with 1.0 mM Ca 2þ than control RyR2 (P o was 5X greater in diabetic RyR2). Two weeks of in... more extent with 1.0 mM Ca 2þ than control RyR2 (P o was 5X greater in diabetic RyR2). Two weeks of insulin treatment blunted the enhanced Ca 2þ responsiveness. When added to the cis chamber the potent reactive carbonyl species (RCS), 80 mM methylglyoxal increased the open probability (P o ) of RyR2 3fold (0.05 to 0.16) within 10 min and this increase was independent of holding potential. Increasing [MGO] further to 160 mM, reduced the conductance of RyR2 by 25% without changing P o . Incubating RyR2 with MGO (5-500 mM with 200 mM free Ca 2þ in buffer) dose-dependently reduced its ability to binding [3H]ryanodine. Singly mutating R1611, R2190 and K2888 to W or Y, to mimic adducts previously found on them during diabetes, resulted in gain-offunction of RyR2 (P o increased >2-fold at 3.3 mM Ca 2þ ). Mutating c-terminal R4462, and R4683 to W or Y resulted in loss-of function of RyR2. We conclude that modification of RyR2 by RCS during diabetes is responsible in part for its dysregulation. (This work was funded by NIH and Nebraska Redox Biology Center)

Mark Turner

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