Michael J. Davies

Bio: Michael J. Davies is an academic researcher from University of Copenhagen. The author has contributed to research in topics: Protein oxidation & Radical. The author has an hindex of 106, co-authored 780 publications receiving 51355 citations. Previous affiliations of Michael J. Davies include University of York & University of Western Australia.

A Novel Method for Measuring Antioxidant Capacity and its Application to Monitoring the Antioxidant Status in Premature Neonates

Abstract: 1. A new method has been developed for measuring the total antioxidant capacity of body fluids and drug solutions, based on the absorbance of the ABTS.+ radical cation. 2. An automated method for use on a centrifugal analyser, as well as a manual method, is described. 3. The procedure has been applied to physiological antioxidant compounds and radical-scavenging drugs, and an antioxidant ranking was established based on their reactivity relative to a 1.0 mmol/l Trolox standard. 4. The Trolox equivalent antioxidant capacity of plasma from an adult reference population has been measured, and the method optimized and validated. 5. The method has been applied to investigate the total plasma antioxidant capacity of neonates and how this may be compromised in prematurity.

Thrombosis and Acute Coronary-Artery Lesions in Sudden Cardiac Ischemic Death

Abstract: The nature of the pathologic lesion in sudden cardiac ischemic death is in dispute. Among 100 subjects who died of ischemic heart disease in less than six hours, coronary thrombi were found in 74. There was no difference in incidence between those who died in less than 15 minutes, those who died in 15 to 60 minutes, and those who died after one hour. Among 26 cases without an intraluminal thrombus, plaque fissuring was found in 21; thus, in only 5 cases was no acute arterial lesion demonstrated. No intraluminal thrombi were found in age-matched controls. Forty-eight of the 74 thrombi were found at sites of preexisting high-grade stenosis; 14 were found at points of previous stenosis of less than 50 per cent of the diameter of the lumen. Forty-seven per cent of the thrombi were found in the right coronary artery. Only 30 per cent were found in the left anterior descending coronary artery. The pathologic process in sudden ischemic death involves a rapidly evolving coronary-artery lesion in which plaque fissuring and resultant thrombus formation are present. These findings have implications for the prevention of sudden cardiac death by antithrombotic therapy.

Biochemistry and pathology of radical-mediated protein oxidation

Abstract: Radical-mediated damage to proteins may be initiated by electron leakage, metal-ion-dependent reactions and autoxidation of lipids and sugars. The consequent protein oxidation is O2-dependent, and involves several propagating radicals, notably alkoxyl radicals. Its products include several categories of reactive species, and a range of stable products whose chemistry is currently being elucidated. Among the reactive products, protein hydroperoxides can generate further radical fluxes on reaction with transition-metal ions; protein-bound reductants (notably dopa) can reduce transition-metal ions and thereby facilitate their reaction with hydroperoxides; and aldehydes may participate in Schiff-base formation and other reactions. Cells can detoxify some of the reactive species, e.g. by reducing protein hydroperoxides to unreactive hydroxides. Oxidized proteins are often functionally inactive and their unfolding is associated with enhanced susceptibility to proteinases. Thus cells can generally remove oxidized proteins by proteolysis. However, certain oxidized proteins are poorly handled by cells, and together with possible alterations in the rate of production of oxidized proteins, this may contribute to the observed accumulation and damaging actions of oxidized proteins during aging and in pathologies such as diabetes, atherosclerosis and neurodegenerative diseases. Protein oxidation may also sometimes play controlling roles in cellular remodelling and cell growth. Proteins are also key targets in defensive cytolysis and in inflammatory self-damage. The possibility of selective protection against protein oxidation (antioxidation) is raised.

The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria

Abstract: Background: Polycystic ovary syndrome (PCOS) is considered to be the most common endocrine disorder in women of reproductive age, yet debate over appropriate diagnostic criteria and design limitations with sampling methodology have left some doubt as to the actual prevalence in the community. The objective of this study was to create a representative prevalence estimate of PCOS in the community under the National Institutes of Health (NIH) criteria and the more recent Rotterdam consensus criteria and Androgen Excess Society (AES) criteria. Methods: A retrospective birth cohort study was carried out in which 728 women born during 1973–1975 in a single maternity hospital were traced and interviewed in adulthood (age = 27–34 year; n = 728). Symptoms of PCOS (hyperandrogenism, menstrual dysfunction and polycystic ovaries) were identified by examination and the presence of polycystic ovaries in those that did not consent to the ultrasound were imputed. Results: The estimated prevalence of PCOS in this birth cohort using the NIH criteria was 8.7 ± 2.0% (with no need for imputation). Under the Rotterdam criteria, the prevalence was 11.9 ± 2.4% which increased to 17.8 ± 2.8% when imputed data were included. Under the AES recommendations, PCOS prevalence was 10.2 ± 2.2%, and 12.0 ± 2.4% with the imputed data. Of the women with PCOS, 68–69% did not have a pre-existing diagnosis. Conclusions: The Rotterdam and AES prevalence estimates were up to twice that obtained with the NIH criteria in this, as well other prevalence studies. In addition, this study also draws attention to the issue of many women with PCOS in the community remaining undiagnosed.

The pathogenesis of atherosclerosis: a perspective for the 1990s

Abstract: Atherosclerosis, the principal cause of heart attack, stroke and gangrene of the extremities, is responsible for 50% of all mortality in the USA, Europe and Japan. The lesions result from an excessive, inflammatory-fibroproliferative response to various forms of insult to the endothelium and smooth muscle of the artery wall. A large number of growth factors, cytokines and vasoregulatory molecules participate in this process. Our ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.