636 research outputs found
Supplemental Material - Cardiometabolic risk factors, peripheral arterial tonometry and metformin in adults with type 1 diabetes participating in the REducing with MetfOrmin Vascular Adverse Lesions trial
No full textSupplemental Material for Cardiometabolic risk factors, peripheral arterial tonometry and metformin in adults with type 1 diabetes participating in the REducing with MetfOrmin Vascular Adverse Lesions trial by David Chen, Alicia J Jenkins, Nicola Greenlaw, Katie Dudman, Tamsin Fernandes, David M Carty, Alun D Hughes, Andrzej S Januszewski, Coen DA Stehouwer and John R Petrie in Diabetes and Vascular Disease Research</p
Body mass index and height from infancy to adulthood and carotid intima-media thickness at 60 to 64 years in the 1946 British Birth cohort study
No full textOBJECTIVE - : Atherosclerosis begins early in life and obesity is a key determinant. We investigated the role of body mass index (BMI) and height from infancy to adulthood in presenting with high adulthood carotid intima-media thickness. APPROACH AND RESULTS - : Odds ratios of BMI, and height Z scores at 2, 4, 6, 7, 11, 15, and 20 years, and changes between 2 and 4, 4 and 7, 7 and 15, and 15 and 20 years, for carotid intima-media thickness at 60 to 64 years in the upper quartile were estimated for 604 men and 669 women. Confounding by early-life environments, mediating by body size and cardiometabolic measures at 60 to 64 years, and effect modification were investigated. In men, there was positive association of BMI at 4 years (odds ratio, 1.256; 95% confidence interval, 1.026-1.538) and 20 years (1.282; 1.022-1.609), negative association of height at 4 years (0.780; 0.631-0.964), and negative association of height growth between 2 and 4 years (0.698; 0.534-0.913) with high carotid intima-media thickness. The childhood estimates were robust, but the estimate for BMI at 20 years was attenuated by adjustment for BMI at 60 to 64 years. The protective influence of greater early childhood height was strongest in those with the lowest systolic blood pressure at 60 to 64 years. In women, there was no pattern of association and all confidence intervals crossed 1. CONCLUSIONS - : Early childhood in men might be a sensitive developmental period for atherosclerosis, in which changes in BMI and height represent 2 distinct biological mechanisms. The maintenance of healthy weight in men from adolescence onward may be a useful strategy to avoid the atherosclerotic complications of adiposity tracking.</p
Angiographic functional scoring of coronary artery disease predicts mortality in patients with severe aortic stenosis undergoing TAVR
No full textAbstract not availableMichael Michail, Udit Thakur, Andrea Comella, Ren Y. Lim, Vivek Gupta, Sean Tan, Hashrul Rashid, James D. Cameron, Stephen J. Nicholls, Liam M. McCormick, Robert P. Gooley, Anthony Mathur, Alun D. Hughes, Adam J. Brow
Timed exercise stabilizes behavioral rhythms but not molecular programs in the brain’s suprachiasmatic clock
Get PDFTimed daily access to a running-wheel (scheduled voluntary exercise; SVE) synchronizes rodent circadian rhythms and promotes stable, 24h rhythms in animals with genetically targeted impairment of neuropeptide signaling (Vipr2 -/- mice). Here we used RNA-seq and/or qRT-PCR to assess how this neuropeptide signaling impairment as well as SVE shapes molecular programs in the brain clock (suprachiasmatic nuclei; SCN) and peripheral tissues (liver and lung). Compared to Vipr2 +/+ animals, the SCN transcriptome of Vipr2 -/- mice showed extensive dysregulation which included core clock components, transcription factors, and neurochemicals. Furthermore, although SVE stabilized behavioral rhythms in these animals, the SCN transcriptome remained dysregulated. The molecular programs in the lung and liver of Vipr2 -/- mice were partially intact, although their response to SVE differed to that of these peripheral tissues in the Vipr2 +/+ mice. These findings highlight that SVE can correct behavioral abnormalities in circadian rhythms without causing large scale alterations to the SCN transcriptome.</p
Patterns of adiposity, vascular phenotypes and cognitive function in the 1946 British Birth Cohort.
Get PDFBACKGROUND: The relationship between long-term exposure to whole body or central obesity and cognitive function, as well as its potential determinants, remain controversial. In this study, we assessed (1) the potential impact of 30 years exposure to different patterns of whole body and central adiposity on cognitive function at 60-64 years, (2) whether trajectories of central adiposity can provide additional information on later cognitive function compared to trajectories of whole body adiposity, and (3) the influence of vascular phenotypes on these associations. METHODS: The study included 1249 participants from the prospective cohort MRC National Survey of Health and Development. Body mass index (BMI), waist circumference (WC), and vascular (carotid intima-media thickness, carotid-femoral pulse wave velocity) and cognitive function (memory, processing speed, reaction time) data, at 60-64 years, were used to assess the associations between different patterns of adult WC or BMI (from 36 years of age) and late midlife cognitive performance, as well as the proportion of this association explained by cardiovascular phenotypes. RESULTS: Longer exposure to elevated WC was related to lower memory performance (p < 0.001 for both) and longer choice reaction time (p = 0.003). A faster gain of WC between 36 and 43 years of age was associated with the largest change in reaction time and memory test (P < 0.05 for all). Similar associations were observed when patterns of WC were substituted with patterns of BMI, but when WC and BMI were included in the same model, only patterns of WC remained significantly associated with cognitive function. Participants who dropped one BMI category and maintained a lower BMI had similar memory performance to those of normal weight during the whole follow-up. Conversely, those who dropped and subsequently regained one BMI category had a memory function similar to those with 30 years exposure to elevated BMI. Adjustment for vascular phenotypes, levels of cardiovascular risk factors, physical activity, education, childhood cognition and socioeconomic position did not affect these associations. CONCLUSIONS: Longer exposure to elevated WC or BMI and faster WC or BMI gains between 36 and 43 years are related to lower cognitive function at 60-64 years. Patterns of WC in adulthood could provide additional information in predicting late midlife cognitive function than patterns of BMI. The acquisition of an adverse cardiovascular phenotype associated with adiposity is unlikely to account for these relationships
4C.01: LIFETIME OBESITY, CARDIOVASCULAR DISEASE AND COGNITIVE FUNCTION: A LONGITUDINAL STUDY FROM THE 1946 BIRTH COHORT
No full textObesity is a major risk factor for cognitive impairment and increases risk of cardiovascular disease (CVD). As CVD in itself is a risk factor for cognitive impairment, we assessed the influence of cardiovascular (CV) phenotypes on the association between lifetime exposure to obesity and midlife memory function.(Figure is included in full-text article.
One Pill, Four Questions: What we Still need to Know about Reducing Cardiovascular Risk with Combination Therapy
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