148 research outputs found

    Adopting and maintaining a healthy lifestyle in low SES families: How the experience of motherhood shapes responses to dietary and physical activity public health guidance

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    Availability of data and materials: The data that support the findings of this study are available in the PhD thesis, Wittels PY Shaping health: understanding and influencing lifestyle behaviours in low socioeconomic women, Brunel University London, 2021 https://bura.brunel.ac.uk/bitstream/2438/21644/1/FulltextThesis.pdf.The Annette Lawson (AL) Charitable Trust made an award of £600 with the funds being used to recognise the time the participants gave to the interviews. Brunel University College of Health and Life Sciences made an award of an additional £200 to make payments to the participants for the third interviews

    The Family Is My Priority: How Motherhood Frames Participation in Physical Activity in a Group of Mothers Living in a Low Socioeconomic Status Area

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    Copyright: © 2022 by the authors. Socioeconomic status (SES) is known to influence strongly both life expectancy and healthy life expectancy. Whilst there are multiple factors with complex interactions that provide the explanation for this observation, differences in the uptake of physical activity between high and low SES groups play a role. This in-depth qualitative study set out to understand the response of a group of mothers with young children living in a low SES area of a London (UK) borough to the current physical activity guidance and to investigate whether existing and established interventions based on behavior change are appropriate for this group. A series of three in depth interviews was carried out with the mothers (n = 20) over a period of 16 months, and the data collected were analyzed thematically. Four main themes were identified: (1) mothering comes before exercise; (2) mothers are a special case; (3) alone or together; and (4) facilities fail mothers. The mothers were unsure about the benefits of exercise, whether it was relevant for them and how to accommodate exercise alongside their mothering responsibilities. Family and peer group could be both a barrier and a facilitator to participation in physical activity. Without an in depth understanding of the role of physical activity in the lives of mothers of young children, behavior change-based public interventions are likely to fail to meet the needs of this group. A reduction in the current health inequities will only be possible when the needs of the mothers are acknowledged and used as the basis of appropriate public health guidance.The Annette Lawson (AL) Charitable Trust; Brunel University London, College of Health and Life Sciences

    Genes of cell-cell interactions, chemotherapy detoxification and apoptosis are induced during chemotherapy of acute myeloid leukemia

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    <p>Abstract</p> <p>Background</p> <p>The molecular changes <it>in vivo </it>in acute myeloid leukemia cells early after start of conventional genotoxic chemotherapy are incompletely understood, and it is not known if early molecular modulations reflect clinical response.</p> <p>Methods</p> <p>The gene expression was examined by whole genome 44 k oligo microarrays and 12 k cDNA microarrays in peripheral blood leukocytes collected from seven leukemia patients before treatment, 2–4 h and 18–24 h after start of chemotherapy and validated by real-time quantitative PCR. Statistically significantly upregulated genes were classified using gene ontology (GO) terms. Parallel samples were examined by flow cytometry for apoptosis by annexin V-binding and the expression of selected proteins were confirmed by immunoblotting.</p> <p>Results</p> <p>Significant differential modulation of 151 genes were found at 4 h after start of induction therapy with cytarabine and anthracycline, including significant overexpression of 31 genes associated with p53 regulation. Within 4 h of chemotherapy the BCL2/BAX and BCL2/PUMA ratio were attenuated in proapoptotic direction. FLT3 mutations indicated that non-responders (5/7 patients, 8 versus 49 months survival) are characterized by a unique gene response profile before and at 4 h. At 18–24 h after chemotherapy, the gene expression of p53 target genes was attenuated, while genes involved in chemoresistance, cytarabine detoxification, chemokine networks and T cell receptor were prominent. No signs of apoptosis were observed in the collected cells, suggesting the treated patients as a physiological source of pre-apoptotic cells.</p> <p>Conclusion</p> <p>Pre-apoptotic gene expression can be monitored within hours after start of chemotherapy in patients with acute myeloid leukemia, and may be useful in future determination of therapy responders. The low number of patients and the heterogeneity of acute myeloid leukemia limited the identification of gene expression predictive of therapy response. Therapy-induced gene expression reflects the complex biological processes involved in clinical cancer cell eradication and should be explored for future enhancement of therapy.</p

    Cost-Effectiveness of New Cardiac and Vascular Rehabilitation Strategies for Patients with Coronary Artery Disease

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    Objective: Peripheral arterial disease (PAD) often hinders the cardiac rehabilitation program. The aim of this study was evaluating the relative cost-effectiveness of new rehabilitation strategies which include the diagnosis and treatment of PAD in patients with coronary artery disease (CAD) undergoing cardiac rehabilitation. Data Sources: Best-available evidence was retrieved from literature and combined with primary data from 231 patients. Methods: We developed a Markov decision model to compare the following treatment strategies: 1. cardiac rehabilitation only; 2. ankle-brachial index (ABI) if cardiac rehabilitation fails followed by diagnostic work-up and revascularization for PAD if needed; 3. ABI prior to cardiac rehabilitation followed by diagnostic work-up and revascularization for PAD if needed. Quality-adjusted-life years (QALYs), life-time costs (US ),incrementalcost−effectivenessratios(ICER),andgaininnethealthbenefits(NHB)inQALYequivalentswerecalculated.Athresholdwillingness−to−payof), incremental cost-effectiveness ratios (ICER), and gain in net health benefits (NHB) in QALY equivalents were calculated. A threshold willingness-to-pay of 75 000 was used. Results: ABI if cardiac rehabilitation fails was the most favorable strategy with an ICER of 44251perQALYgainedandanincrementalNHBcomparedtocardiacrehabilitationonlyof0.03QALYs(9544 251 per QALY gained and an incremental NHB compared to cardiac rehabilitation only of 0.03 QALYs (95% CI: −0.17, 0.29) at a threshold willingness-to-pay of 75 000/QALY. After sensitivity analysis, a combined cardiac and vascular rehabilitation program increased the success rate and would dominate the other two strategies with total lifetime costs of $30 246 a quality-adjusted life expectancy of 3.84 years, and an incremental NHB of 0.06 QALYs (95%CI:−0.24, 0.46) compared to current practice. The results were robust for other different input parameters. Conclusion: ABI measurement if cardiac rehabilitation fails followed by a diagnostic work-up and revascularization for PAD if needed are potentially cost-effective compared to cardiac rehabilitation only

    Models of chronic obstructive pulmonary disease

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    Chronic obstructive pulmonary disease (COPD) is a major global health problem and is predicted to become the third most common cause of death by 2020. Apart from the important preventive steps of smoking cessation, there are no other specific treatments for COPD that are as effective in reversing the condition, and therefore there is a need to understand the pathophysiological mechanisms that could lead to new therapeutic strategies. The development of experimental models will help to dissect these mechanisms at the cellular and molecular level. COPD is a disease characterized by progressive airflow obstruction of the peripheral airways, associated with lung inflammation, emphysema and mucus hypersecretion. Different approaches to mimic COPD have been developed but are limited in comparison to models of allergic asthma. COPD models usually do not mimic the major features of human COPD and are commonly based on the induction of COPD-like lesions in the lungs and airways using noxious inhalants such as tobacco smoke, nitrogen dioxide, or sulfur dioxide. Depending on the duration and intensity of exposure, these noxious stimuli induce signs of chronic inflammation and airway remodelling. Emphysema can be achieved by combining such exposure with instillation of tissue-degrading enzymes. Other approaches are based on genetically-targeted mice which develop COPD-like lesions with emphysema, and such mice provide deep insights into pathophysiological mechanisms. Future approaches should aim to mimic irreversible airflow obstruction, associated with cough and sputum production, with the possibility of inducing exacerbations

    Humblebragging: A Distinct And Ineffective Self-Presentation Strategy

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