John R. Mercer

ORCID: 0000-0002-3204-7511
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About
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Research Areas
  • Radiopharmaceutical Chemistry and Applications
  • Cancer, Hypoxia, and Metabolism
  • Medical Imaging Techniques and Applications
  • Mitochondrial Function and Pathology
  • Cancer, Lipids, and Metabolism
  • Cancer Research and Treatments
  • Advanced biosensing and bioanalysis techniques
  • Wireless Power Transfer Systems
  • Bone health and treatments
  • Atherosclerosis and Cardiovascular Diseases
  • Cancer-related Molecular Pathways
  • Wireless Body Area Networks
  • Medical Imaging and Pathology Studies
  • Energy Harvesting in Wireless Networks
  • Neuroscience and Neural Engineering
  • DNA and Nucleic Acid Chemistry
  • Cell death mechanisms and regulation
  • Advanced Chemical Physics Studies
  • RNA Interference and Gene Delivery
  • Metabolism and Genetic Disorders
  • X-ray Diffraction in Crystallography
  • RNA modifications and cancer
  • Analytical Chemistry and Sensors
  • 3D Printing in Biomedical Research
  • Chemical Synthesis and Analysis

University of Glasgow
2016-2025

British Heart Foundation
2022-2024

University of Alberta
2008-2022

University of Cambridge
1982-2014

Addenbrooke's Hospital
2006-2014

MRC Mitochondrial Biology Unit
2010-2013

Level (Czechia)
2013

Papworth Hospital
2007-2013

Medical Research Council
2010

Harvard University Press
2004

Mitochondrial DNA (mtDNA) damage occurs in both circulating cells and the vessel wall human atherosclerosis. However, it is unclear whether mtDNA directly promotes atherogenesis or a consequence of tissue damage, which cell types are involved, its effects mediated only through reactive oxygen species.mtDNA occurred early apolipoprotein E-null (ApoE(-/-)) mice, before significant atherosclerosis developed. defects were also identified monocytes liver associated with mitochondrial dysfunction....

10.1161/circulationaha.113.002271 article EN Circulation 2013-07-11

Vascular smooth muscle cells (VSMCs) in human atherosclerosis manifest extensive DNA damage and activation of the response, a pathway that coordinates cell cycle arrest repair, or can trigger apoptosis senescence. Sirtuin 1 deacetylase (SIRT1) regulates ageing energy metabolism response through multiple targets. However, direct role SIRT1 how VSMCs might regulate are unknown.SIRT1 expression was reduced atherosclerotic plaques both derived from undergoing replicative inhibition repair...

10.1161/circulationaha.112.124404 article EN Circulation 2012-12-08

Abstract Cardiovascular disease continues to be one of the dominant causes global mortality. One effective treatment is utilize cardiovascular implantable devices (cIMDs) with multi‐functional cell sensing and monitoring features that have potential manipulate hyperplasia disorders as well provide therapy. However, batteries a fixed capacity entail high‐risk surgeries for battery‐replacement, which health hazards imposes significant costs patients. This review accesses comprehensive power...

10.1002/admt.202101086 article EN cc-by Advanced Materials Technologies 2022-01-07

Surface x-ray diffraction has been used to determine the structural relaxations of ${\mathrm{TiO}}_{2}(110)\ensuremath{-}(1\ifmmode\times\else\texttimes\fi{}1)$. The magnitudes range from 0 0.27 \AA{}, leading rumpling titanium planes. data are compared results three independent calculations energy minimized structure. Excellent agreement is achieved with positions atoms predicted by Ramamoorthy et al. [Phys. Rev. B 49, 16 721 (1994)].

10.1103/physrevlett.78.495 article EN Physical Review Letters 1997-01-20

Although monocytes/macrophages are considered important in atherogenesis, their role established plaques is unclear. For example, macrophage content associated with plaque instability, but loss through cell death observed at sites of rupture. To examine the atherosclerosis, we developed CD11b–diphtheria toxin (DT) receptor (DTR) transgenic mice, whereby administration DT selectively kills monocytes/macrophages. treatment reduced peripheral blood monocytes and tissue macrophages inhibited...

10.1161/01.res.0000260802.75766.00 article EN Circulation Research 2007-02-23

DNA damage is present in both genomic and mitochondrial atherosclerosis. However, whether itself promotes atherosclerosis, or simply a byproduct of the risk factors that promote unknown.To examine effect on we studied apolipoprotein (Apo)E(-/-) mice were haploinsufficient for protein kinase ATM (ataxia telangiectasia mutated), which coordinates repair.ATM(+/-)/ApoE(-/-) developed accelerated atherosclerosis multiple features metabolic syndrome, including hypertension, hypercholesterolemia,...

10.1161/circresaha.110.218966 article EN Circulation Research 2010-08-13

DNA damage and the response have been identified in human atherosclerosis, including vascular smooth muscle cells (VSMCs). However, although double-stranded breaks (DSBs) are hypothesized to promote plaque progression instability, part, by promoting cell senescence, apoptosis, inflammation, direct effects of DSBs VSMCs seen atherogenesis unknown.To determine presence effect endogenous levels on atherosclerosis.Human atherosclerotic showed increased expression multiple proteins vitro vivo,...

10.1161/circresaha.116.304921 article EN Circulation Research 2014-12-19

Arteriovenous grafts (AVGs) are indispensable life-saving implants for chronic kidney disease (CKD) patients undergoing hemodialysis. However, AVGs will often fail due to postoperative complications such as cellular accumulation termed restenosis, blood clots, and infections, which dominant causes of morbidity mortality. A new generation hemodialysis equipped with biosensors multi-band antennas wireless power telemetry systems that can detect specific pathological parameters report AVGs'...

10.1109/tap.2023.3266786 article EN cc-by IEEE Transactions on Antennas and Propagation 2023-04-18

Recent studies have indicated that the tumor suppressor gene p53 limits atherosclerosis in animal models; expression is also increased advanced human plaques compared with normal vessels, where it may induce growth arrest and apoptosis. However, controversy exists as to role of endogenous levels different cell types comprise plaques. We examined atherosclerotic plaque development composition brachiocephalic arteries aortas p53-/-/ApoE-/- mice versus wild type controls. p53-/- demonstrated...

10.1161/01.res.0000161069.15577.ca article EN Circulation Research 2005-03-04

Although the hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) are widely used in atherosclerosis to reduce serum cholesterol, statins have multiple other effects, including direct effects on cells of vessel wall. Recently, DNA damage, telomere shortening, has been identified vascular smooth muscle (VSMCs) human atherosclerosis. damage vitro, mechanisms by which they might protect integrity VSMCs unknown. We show that atherosclerotic plaque exhibit increased levels...

10.1161/circresaha.108.182899 article EN Circulation Research 2008-08-22

DNA damage and mitochondrial dysfunction are thought to play an essential role in ageing the energetic decline of vascular smooth muscle cells (VSMCs) for maintaining plaque integrity. We aimed better understand VSMCs identify potentially useful compensatory pathways that could extend their lifespan. Moreover, we wanted assess if defects respiration exist human atherosclerotic plaques appropriate markers may reflect a switch VSMC energy metabolism.Human tissue were assessed composition...

10.1016/j.atherosclerosis.2017.11.009 article EN cc-by Atherosclerosis 2017-11-13

This study illustrates the utility of a mixed-methods approach in assessing value an example novel technology-biosensor-integrated self-reporting arteriovenous grafts (smart AVGs). Currently preclinical development, device will detect graft stenosis (surveillance-only use case) and treat (interventional case). The to assessment adopted this was multifaceted, with one stage informing next comprised stakeholder engagement clinical experts explore device's value, cost-utility analysis (CUA)...

10.3390/jmahp13010001 article EN cc-by Journal of Market Access & Health Policy 2025-01-15

<sup>18</sup>F-3′-Deoxy-3′-fluorothymidine (<sup>18</sup>F-FLT) is a PET tracer that accumulates in proliferating tissues. The current study was undertaken to determine whether equilibrative nucleoside transporter 1 (ENT1) important for <sup>18</sup>F-FLT uptake normal tissues and tumors. <b>Methods:</b> ENT1-knockout (ENT1<sup>−/−</sup>) mice were generated compared with wild-type (ENT1<sup>+/+</sup>) using small-animal PET. In addition, ENT1<sup>+/+</sup> also injected the ENT1 inhibitor...

10.2967/jnumed.110.076356 article EN Journal of Nuclear Medicine 2010-08-18
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