Publications by authors named "Sophia D Amenyah"

Background: Obesity and unemployment are complex social and health issues with underlying causes that are interconnected. While a clear link has been established, there is lack of evidence on the underlying causal pathways and how health-related interventions could reduce obesity and unemployment using a holistic approach.

Objectives: The aim of this realist synthesis was to identify the common strategies used by health-related interventions to reduce obesity, overweight and unemployment and to determine for whom and under what circumstances these interventions were successful or unsuccessful and why.

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We previously demonstrated that increased monoclonal antibody productivity in dihydrofolate reductase (DHFR)-amplified CHO cells correlates with phosphorylated transcription factor-cytomegalovirus (CMV) promoter interactions. In this article, we extend the characterization to include CMV promoter methylation and its influence on NFκB and CREB1 transcription factor binding to the CMV promoter in two families of DHFR-amplified CHO cell lines. CMV promoter methylation was determined using bisulfite sequencing.

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Background: Obesity, overweight and unemployment are interlinked, with debilitating effects on mortality, health, wellbeing and quality of life. Existing interventions to reduce overweight, obesity and unemployment have addressed these challenges independent of each other with limited success. The Adding to Social capital and individual Potential In disadvantaged REgions (ASPIRE) project will develop an innovative model using a combination of skills training and health and wellbeing interventions to improve health, wellbeing, quality of life and reduce overweight, obesity and unemployment in England and France.

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Background: The interaction between genetic, epigenetic and environmental factors plays an important role in the aetiology of hypertension. GWAS and observational studies link the C677T polymorphism in methylenetetrahydrofolate reductase (MTHFR) with hypertension, while riboflavin, the MTHFR cofactor, has been shown to reduce blood pressure and global DNA methylation in homozygous (TT genotype) individuals. It is currently unclear whether riboflavin modulates DNA methylation of other hypertension-related genes.

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Recent advances in epigenetic research have enabled the development of epigenetic clocks, which have greatly enhanced our ability to investigate molecular processes that contribute to aging and age-related disease. These biomarkers offer the potential to measure the effect of environmental exposures linked to dynamic changes in DNA methylation, including nutrients, as factors in age-related disease. They also offer a compelling insight into how imbalances in the supply of nutrients, particularly B-vitamins, or polymorphisms in regulatory enzymes involved in 1-carbon metabolism, the key pathway that supplies methyl groups for epigenetic reactions, may influence epigenetic age and interindividual disease susceptibility.

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DNA methylation is important in regulating gene expression and genomic stability while aberrant DNA methylation is associated with disease. Riboflavin (FAD) is a cofactor for methylenetetrahydrofolate reductase (MTHFR), a critical enzyme in folate recycling, which generates methyl groups for homocysteine remethylation to methionine, the pre-cursor to the universal methyl donor S-adenosylmethionine (SAM). A polymorphism (C677T) in MTHFR results in decreased MTHFR activity and increased homocysteine concentration.

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Context: Aberrant DNA methylation is linked to various diseases. The supply of methyl groups for methylation reactions is mediated by S-adenosylmethionine, which depends on the availability of folate and related B vitamins.

Objectives: To investigate the influence of key nutrients involved in 1-carbon metabolism on DNA methylation in adults.

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