Publications by authors named "B P Setchell"

216 Publications

Pressure injury and risk in the inpatient paediatric and neonatal populations: A single centre point-prevalence study.

J Tissue Viability 2021 May 9;30(2):231-236. Epub 2021 Feb 9.

Nottingham Childrens Hospital and Neonatal Services, Family Health Division, Nottingham University Hospitals NHS Trust, Nottingham, UK; Children and Young People Health Research, School of Health Sciences, University of Nottingham, Nottingham, UK.

Introduction: Prevention and management of pressure injury is a key nurse-sensitive quality indicator. From clinical insights, pressure injury effects hospitalised neonates and children, however it is unclear how prevalent this is. The aim of this study was to quantify prevalence of pressure injury, assess skin integrity risk level, and quantify preventive interventions in both neonatal and child inpatient populations at a large children's hospital in the UK.

Methods: A cross-sectional study was undertaken, assessing the skin integrity of all children allocated to a paediatric or neonatal bed in June/July 2020. A data collection tool was adapted from two established pressure ulcer point prevalence surveys (EUPAP and Medstrom pre-prevalence survey). Risk assessment was performed using the Braden QD scale.

Results: Eighty-eight participants were included, with median age of 0.85 years [range 0-17.5 years), with 32 (36%) of participants being preterm. Median length of hospital stay was 11 days [range 0-174 days]. Pressure ulcer prevalence was 3.4%. The majority of participants had at least two medical devices, with 16 (18.2%) having more than four. Having a medical device was associated with increased risk score of developing pressure injury (odds ratio [OR] 0.03, 95% Confidence Interval [CI] 0.01-0.05, p = 0.02). Most children (39 (44%)) were reported not having proposed preventive measures in place aligned to their risk assessment. However, for those that did, 2 to 4 hourly repositioning was associated with a risk reduction on pressure damage (OR 0.13, 95% CI 0.03-0.23, p = 0.01).

Conclusion: Overall, we found a low prevalence of pressure injury across preterm infants, children and young people at a tertiary children's hospital. Accurate risk assessment as well as availability and implementation of preventive interventions are a priority for healthcare institutes to avoid pressure injury.
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http://dx.doi.org/10.1016/j.jtv.2021.02.004DOI Listing
May 2021

Effects of whole-body heat on male germ cell development and sperm motility in the laboratory mouse.

Reprod Fertil Dev 2016 Apr;28(5):545-55

Discipline of Anatomy and Pathology, School of Medical Sciences, Faculty of Health Sciences, University of Adelaide, Adelaide, SA 5005, Australia.

This study investigated the effects of high temperatures on male germ cell development and epididymal sperm motility of laboratory mice. In Experiment 1, adult males (n=16) were exposed to whole-body heat of 37-38°C for 8h day(-1) for 3 consecutive days, whereas controls (n=4) were left at 23-24°C. In Experiment 2, adult mice (n=6) were exposed to 37-38°C for a single 8-h period with controls (n=6) left at 23-24°C. Experiment 2 was conducted as a continuation of previous study that showed changes in spermatozoa 16h after exposure to heat of 37-38°C for 8h day(-1) for 3 consecutive days. In the present study, in Experiment 1, high temperature reduced testes weights 16h and 14 days after exposure, whereas by Day 21 testes weights were similar to those in the control group (P=0.18). At 16h, 7 and 14 days after exposure, an increase in germ cell apoptosis was noticeable in early and late stages (I-VI and XI-XII) of the cycle of the seminiferous epithelium. However, apoptosis in intermediate stages (VII-X) was evident 16h after heat exposure (P<0.05), without any change at other time periods. By 21 days, there were no significant differences between heat-treated groups and controls. Considerably more caspase-3-positive germ cells occurred in heat-treated mice 16h after heat exposure compared with the control group (P<0.0001), whereas 8h after heat in Experiment 2, sperm motility was reduced with a higher percentage of spermatozoa showing membrane damage. In conclusion, the present study shows that whole-body heat of 37-38°C induces stage-specific germ cell apoptosis and membrane changes in spermatozoa; this may result in reduced fertility at particular times of exposure after heating.
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http://dx.doi.org/10.1071/RD13395DOI Listing
April 2016

Obese father's metabolic state, adiposity, and reproductive capacity indicate son's reproductive health.

Fertil Steril 2014 Mar 11;101(3):865-73. Epub 2014 Jan 11.

Discipline of Obstetrics and Gynaecology, School of Paediatrics and Reproductive Health, Robinson Institute, The University of Adelaide, Adelaide, South Australia, Australia; Repromed, Dulwich, South Australia, Australia.

Objective: To determine whether dietary and exercise regimes in obese males can provide a novel intervention window for improving the reproductive health of the next generation.

Design: Experimental animal study.

Setting: University research facilities.

Animal(s): C57BL6 male and female mice.

Intervention(s): Mice were fed a control diet (6% fat) or high-fat diet (21% fat) for 9 weeks. After the initial feeding, high-fat-diet males were allocated to diet and/or exercise interventions for a further 9 weeks. After intervention males were mated with females fed standard chow (4% fat) before and during pregnancy.

Main Outcome Measure(s): F1 sperm motility, count, morphology, capacitation, mitochondrial function, and sperm binding and weight of reproductive organs.

Result(s): Our primary finding was that diet intervention alone in founders improved offspring sperm motility and mitochondrial markers of sperm health (decreased reactive oxygen species and mitochondrial membrane potential), ultimately improving sperm binding. Sperm binding and capacitation was also improved in F1 males born to a combined diet and exercise intervention in founders. Founder sperm parameters and metabolic measures as a response to diet and/or exercise (i.e., lipid/glucose homeostasis, sperm count and morphology) correlated with offspring's sperm function, independent of founder treatment. This implicates paternal metabolic and reproductive status in predicting male offspring's reproductive function.

Conclusion(s): This is the first study to show that improvements to both metabolic (lipids, glucose and insulin sensitivity) and reproductive function (sperm motility and morphology) in obese fathers via diet and exercise interventions can improve subsequent reproductive health in offspring.
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http://dx.doi.org/10.1016/j.fertnstert.2013.12.007DOI Listing
March 2014

Improving metabolic health in obese male mice via diet and exercise restores embryo development and fetal growth.

PLoS One 2013 19;8(8):e71459. Epub 2013 Aug 19.

School of Paediatrics and Reproductive Health, Discipline of Obstetrics and Gynaecology, University of Adelaide, South Australia, Australia.

Paternal obesity is now clearly associated with or causal of impaired embryo and fetal development and reduced pregnancy rates in humans and rodents. This appears to be a result of reduced blastocyst potential. Whether these adverse embryo and fetal outcomes can be ameliorated by interventions to reduce paternal obesity has not been established. Here, male mice fed a high fat diet (HFD) to induce obesity were used, to determine if early embryo and fetal development is improved by interventions of diet (CD) and/or exercise to reduce adiposity and improve metabolism. Exercise and to a lesser extent CD in obese males improved embryo development rates, with increased cell to cell contacts in the compacting embryo measured by E-cadherin in exercise interventions and subsequently, increased blastocyst trophectoderm (TE), inner cell mass (ICM) and epiblast cell numbers. Implantation rates and fetal development from resulting blastocysts were also improved by exercise in obese males. Additionally, all interventions to obese males increased fetal weight, with CD alone and exercise alone, also increasing fetal crown-rump length. Measures of embryo and fetal development correlated with paternal measures of glycaemia, insulin action and serum lipids regardless of paternal adiposity or intervention, suggesting a link between paternal metabolic health and subsequent embryo and fetal development. This is the first study to show that improvements to metabolic health of obese males through diet and exercise can improve embryo and fetal development, suggesting such interventions are likely to improve offspring health.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0071459PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3747240PMC
April 2014

Diet and exercise in an obese mouse fed a high-fat diet improve metabolic health and reverse perturbed sperm function.

Am J Physiol Endocrinol Metab 2012 Apr 17;302(7):E768-80. Epub 2012 Jan 17.

School of Paediatrics and Reproductive Health, Discipline of Obstetrics and Gynaecology, University of Adelaide, South Australia, Australia.

Male obesity is associated with reduced sperm motility and morphology and increased sperm DNA damage and oxidative stress; however, the reversibility of these phenotypes has never been studied. Therefore, the aim of this study was to assess the reversibility of obesity and its associated sperm physiology and function in mice in response to weight loss through diet and exercise. C57BL6 male mice (n = 40) were fed either a control diet (CD; 6% fat) or a high-fat diet (HFD; 21% fat) for 10 wk before allocation to either diet and/or swimming exercise interventions for 8 wk. Diet alone reduced adiposity (1.6-fold) and serum cholesterol levels (1.7-fold, P < 0.05), while exercise alone did not alter these, but exercise plus diet also improved glucose tolerance (1.3-fold, P < 0.05). Diet and/or exercise improved sperm motility (1.2-fold) and morphology (1.1-fold, P < 0.05), and reduced sperm DNA damage (1.5-fold), reactive oxygen species (1.1-fold), and mitochondrial membrane potential (1.2-fold, P < 0.05) and increased sperm binding (1.4-fold) (P < 0.05). Sperm parameters were highly correlated with measures of glycemia, insulin action, and serum cholesterol (all P < 0.05) regardless of adiposity or intervention, suggesting a link between systemic metabolic status and sperm function. This is the first study to show that the abnormal sperm physiology resulting from obesity can be reversed through diet and exercise, even in the presence of ongoing obesity, suggesting that diet and lifestyle interventions could be a combined approach to target subfertility in overweight and obese men.
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http://dx.doi.org/10.1152/ajpendo.00401.2011DOI Listing
April 2012
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