Publications by authors named "A F Riddell"

Background: Acquired haemophilia A (AHA) is an acquired bleeding disorder resulting from autoantibodies against Factor VIII (FVIII). Previous studies have reported differences in FVIII inhibitor kinetics (type I or type II) in AHA compared to severe haemophilia A.

Aim: To characterise inhibitor kinetics in AHA and evaluate the proportions displaying type I, II or indeterminate kinetics.

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Introduction: Acute liver failure (ALF) has no effective treatment other than liver transplantation and is commonly caused by paracetamol overdose. New treatments are needed to treat and prevent ALF. Alternatively-activated macrophages (AAMs) can promote resolution of liver necrosis and stimulate hepatocyte proliferation.

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Aim: To assess the diagnostic accuracy and inter-reader agreement of a simulated abbreviated gadoxetate liver magnetic resonance imaging (MRI) protocol together with contrast-enhanced computed tomography (CE-CT) against a standard gadoxetate MRI for the detection of colorectal liver metastases at baseline.

Materials And Methods: Three readers independently evaluated two sets of images per patient, recording number and location of metastases and benign lesions. Set 1 comprised T1w, T2w, DWI, multiphase CE-T1w, and hepatobiliary phase (HBP) images (standard).

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Article Synopsis
  • Symmetric dimethylarginine (SDMA) is a by-product of cellular metabolism linked to endothelial dysfunction and vascular risk, challenging its previously considered inert status.
  • The review focuses on SDMA's role in cerebrovascular diseases, particularly ischaemic stroke, examining its impact on factors like nitric oxide signaling, inflammation, and oxidative stress.
  • Recent studies indicate a correlation between elevated SDMA levels and poor outcomes in stroke patients, emphasizing the need for further research to understand SDMA's potential as both a marker and mediator of cerebrovascular disease.
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Introduction: Factor (F) XI deficiency is an inherited bleeding disorder with increased prevalence in Ashkenazi Jews where it is mainly caused by two variants, p.Glu135* (type II, leading to a null allele) and p.Phe301Leu (type III, missense variant).

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