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Adam Michael Taylor

Researcher at Lancaster University

Publications -  48
Citations -  745

Adam Michael Taylor is an academic researcher from Lancaster University. The author has contributed to research in topics: Alkaptonuria & Ochronosis. The author has an hindex of 13, co-authored 46 publications receiving 655 citations. Previous affiliations of Adam Michael Taylor include University of Liverpool & Royal Liverpool and Broadgreen University Hospital NHS Trust.

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The role of calcified cartilage and subchondral bone in the initiation and progression of ochronotic arthropathy in alkaptonuria

TL;DR: Using alkaptonuria cartilage specimens with a wide spectrum of pigmentation, the progression of ochronosis is characterized and should contribute to better understanding of cartilage-subchondral interactions in arthropathies.
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Ochronotic osteoarthropathy in a mouse model of alkaptonuria, and its inhibition by nitisinone

TL;DR: The AKU mouse was established as a model of both the plasma biochemistry of AKU and its associated arthropathy and the cellular pathology of ochronosis in AKU mice is identical to that observed in early human o Chronosis and thus is a model in which the early stages of joint pathology can be studied and novel interventions evaluated.
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Ultrastructural examination of tissue in a patient with alkaptonuric arthropathy reveals a distinct pattern of binding of ochronotic pigment

TL;DR: A female with known alkaptonuria (AKU) undergoing routine hip replacement surgery due to alkapt onuric arthropathy is reported, which is caused by a deficiency in the enzyme that breaks down homogentisic acid, resulting in elevated circulation of HGA levels in the body.
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Development of an in vitro model to investigate joint ochronosis in alkaptonuria

TL;DR: An in vitro model of ochronosis that should contribute to understanding joint destruction in AKU and to the aetiology of OA is developed, indicating that protective mechanisms exist in tissues in situ.
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Proteomic and redox-proteomic evaluation of homogentisic acid and ascorbic acid effects on human articular chondrocytes.

TL;DR: The hypothesis that HGA‐induced stress might be mediated by protein oxidation is supported and can lay the basis towards the settling up of more sophisticated models to study AKU and ochronosis.