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Spencer N.,Warwick Medical School | Strazdins L.,Australian National University
Archives of Disease in Childhood | Year: 2015

Objective: To study the temporal relationship between socioeconomic disadvantage and onset of chronic disabling conditions in childhood. Method: Using parent reported data from the Longitudinal Study of Australian Children, we compared children who developed a chronic disabling condition between the ages of 6/7 and 10/11 years with children without a chronic disabling condition at either age. Logistic regression models assessed association between onset of chronic disabling condition and household income quintiles at 6/7 years, adjusting for confounders. To study the consequences of chronic disabling condition onset for family finances, a linear regression model was fitted on change in household income adjusted for income at 6/7. We compared prevalence of family material hardship in the two groups between 6/7 and 10/11. Results: Of 4010 children present in both waves, complete data were available for 3629 of whom 233 (6.4%) developed a chronic disabling condition between 6/7 and 10/11. After adjustment for confounding, the children from the lowest income quintile were more than twice as likely to develop a chronic disabling condition as those from the highest income quintile. Onset of a chronic disabling condition was associated with a relatively smaller increase in household income over time, but no change in hardship prevalence. Conclusions: Family socioeconomic disadvantage when children are aged 6/7 is associated with their development of a chronic disabling condition over the next 4 years and with adverse effects on household income. © 2015, BMJ Publishing Group. All rights reserved. Source

Megson M.,Warwick Medical School
BMJ Case Reports | Year: 2011

A 79-year-old female, presented to accident and emergency with a painful right leg from the knee distally, after tripping. On examination, her right lower leg had a haematoma on the anterolateral aspect which was very tender. After 4 days, the patient was taken to theatre for debridement, and the wound was washed out. The next day, the wound was reconstructed with a split skin graft. Source

Cozzolino M.,University of Milan | Ketteler M.,Klinikum Coburg | Zehnder D.,Warwick Medical School
European Journal of Heart Failure | Year: 2010

Chronic kidney disease (CKD) independently increases the rates of cardiovascular disease, whereas the severity of kidney disease correlates with increased cardiovascular morbidity and death. Vitamin D is modified in the liver and the kidney to its active form (1,25-dihydroxyvitamin D) by the 25-hydroxy vitamin D 1-hydroxylase enzyme (CYP27B1). The activated vitamin D brings about its actions through the vitamin D receptor (VDR). The VDRs and CYP27B1 have recently been shown to be expressed in several tissues, not directly involved in mineral homeostasis, including the cardiovascular, immune, and epithelial systems. The action of vitamin D in these tissues is implicated in the regulation of endothelial, vascular smooth muscle, and cardiac cell function, the renin-angiotensin system, inflammatory and fibrotic pathways, and immune response. Impaired VDR activation and signalling results in cellular dysfunction in several organs and biological systems, which leads to reduced bone health, an increased risk for epithelial cancers, metabolic disease, and uncontrolled inflammatory responses. Failure of cardiovascular VDR activation results in hypertension, accelerated atherosclerosis and vascular calcification, cardiac hypertrophy with vascular rarification and fibrosis, and progressive renal dysfunction. An emerging body of evidence has prompted attention to the relationship between CKD, mineral bone disorder (CKD-MBD), and cardiovascular disease in the new guidelines from Kidney Disease: Improving Global Outcomes. Vitamin D receptor activators, commonly used to treat CKD-MBD, and an appropriate treatment of vitamin D hormonal system failure in patients with CKD, may help to reduce cardiovascular morbidity and mortality in these patients. © 2010 The Author. Source

Wollman A.J.M.,University of Oxford | Sanchez-Cano C.,University of Oxford | Carstairs H.M.J.,University of Oxford | Cross R.A.,Warwick Medical School | Turberfield A.J.,University of Oxford
Nature Nanotechnology | Year: 2014

In eukaryotic cells, cargo is transported on self-organized networks of microtubule trackways by kinesin and dynein motor proteins. Synthetic microtubule networks have previously been assembled in vitro, and microtubules have been used as shuttles to carry cargoes on lithographically defined tracks consisting of surface-bound kinesin motors. Here, we show that molecular signals can be used to program both the architecture and the operation of a self-organized transport system that is based on kinesin and microtubules and spans three orders of magnitude in length scale. A single motor protein, dimeric kinesin-1, is conjugated to various DNA nanostructures to accomplish different tasks. Instructions encoded into the DNA sequences are used to direct the assembly of a polar array of microtubules and can be used to control the loading, active concentration and unloading of cargo on this track network, or to trigger the disassembly of the network. © 2014 Macmillan Publishers Limited. Source

Shyangdan D.S.,Warwick Medical School | Uthman O.A.,Center for Applied Health Research and Delivery | Waugh N.,Public Health Medicine and Health Technology Assessment
BMJ Open | Year: 2016

Objective: Because of the lack of head-to-head trials, the aim was to indirectly compare sodium glucose transporter-2 (SGLT-2) inhibitors in the treatment of type 2 diabetes. Design: Systematic review and network meta-analysis. Data sources: MEDLINE and EMBASE were searched from January 2005 to January 2015. Eligibility criteria: Randomised controlled trials assessing the efficacy of SGLT-2 inhibitors in patients with type 2 diabetes inadequately controlled with diet and exercise alone or metformin monotherapy. Minimum duration 24 weeks. Indirect comparison was undertaken using Bayesian methods. Results: In monotherapy, a greater proportion of patients achieved a glycated haemoglobin (HbA1c) level of <7% on canagliflozin 300 mg than on canagliflozin 100 mg (risk ratio (RR) 0.72%, 95% credible intervals (CrI) 0.59% to 0.87%) and dapagliflozin 10 mg (RR 0.63, 95% CrI 0.48 to 0.85) but there were no significant differences compared with either dose of empagliflozin. In monotherapy, canagliflozin 300 mg reduced HbA1c more than other SGLT-2 inhibitors (mean difference ranged from 0.20% to 0.64%). There were no significant differences in weight reduction. All the flozins reduced systolic blood pressure (SBP) more than placebo, ranging from a reduction of 6 mm Hg with canagliflozin 300-2.6 mm Hg with empagliflozin 10 mg. In dual therapy with metformin, all flozins were more effective than placebo for achieving HbA1c <7%, and reducing HbA1c, weight and SBP. The proportions achieving HbA1c level of <7% were mostly similar. Canagliflozin 300 mg reduced HbA1c more than the other drugs but this just reached statistical significance only against canagliflozin 100 mg (MD 0.15, CrI 0.04 to 0.26). Conclusions: There were few differences among the SGLT-2 inhibitors, but in monotherapy, the glucoselowering effect of canagliflozin 300 mg is slightly greater than most other SGLT-2 inhibitors. Source

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