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Aims The aim of this study was to determine whether the sequential application of povidone iodine-alcohol (PVI) followed by chlorhexidine gluconate-alcohol (CHG) would reduce surgical wound contamination to a greater extent than PVI applied twice in patients undergoing spinal surgery. Patients and Methods A single-centre, interventional, two arm, parallel group randomised controlled trial was undertaken, involving 407 patients who underwent elective spinal surgery. For 203 patients, the skin was disinfected before surgery using PVI (10% [w/w (1% w/w available iodine)] in 95% industrial denatured alcohol, povidone iodine; Videne Alcoholic Tincture) twice, and for 204 patients using PVI once followed by CHG (2% [w/v] chlorhexidine gluconate in 70% [v/v] isopropyl alcohol; Chloraprep with tint). The primary outcome measure was contamination of the wound determined by aerobic and anaerobic bacterial growth from samples taken after disinfection. Results The detection of viable bacteria in any one of the samples taken after disinfection (culture-positive) was significantly lower in the group treated with both PVI and CHG than in the group treated with PVI alone (59 (29.1%) versus 85 (41.7%), p = 0.009; odds ratio 0.574; 95% confidence interval, 0.380 to 0.866). Conclusions Antisepsis of the skin with the sequential application of PVI and CHG more effectively reduces the contamination of a surgical wound than PVI alone. Cite this article: Bone Joint J 2017;99-B:1354–65.

Abstract The residential sector accounts for most of energy-consumption in developing countries in the form of traditional energy. The use of commercial energy is nominal and confined mostly to urban areas where fuelwood is already monetized. A model, based on an end-use/process analysis approach, is developed on a spreadsheet, which is capable of simulating scenarios to address issues of increasing traditional energy-demand caused by population growth, sustainable supply capacity of the existing energy resources, potential for development of new and renewable energy resources, technology. This paper is divided into two parts: general energy issues and the modelling approach, and the application of this approach to Nepal in the context of fuelwood-supply sustainability.

Background and purpose:The contribution of endothelin‐1 (ET‐1) to vascular hyper‐reactivity associated with chronic ethanol intake, a major risk factor in several cardiovascular diseases, remains to be investigated.Experimental approach:The biphasic haemodynamic responses to ET‐1 (0.01–0.1 nmol kg−1, i.v.) or to the selective ETB agonist, IRL1620 (0.001–1.0 nmol kg−1, i.v.), with or without ETA or ETB antagonists (BQ123 (c(DTrp‐Dasp‐Pro‐Dval‐Leu)) at 1 and 2.5 mg kg−1 and BQ788 (N‐cis‐2,6‐dimethyl‐piperidinocarbonyl‐L‐γ‐methylleucyl1‐D‐1methoxycarbonyltryptophanyl‐D‐norleucine) at 0.25 mg kg−1, respectively) were tested in anaesthetized rats, after 2 weeks' chronic ethanol treatment. Hepatic parameters and ET receptor protein levels were also determined.Key results:The initial hypotensive responses to ET‐1 or IRL1620 were unaffected by chronic ethanol intake, whereas the subsequent pressor effects induced by ET‐1, but not by IRL1620, were potentiated. BQ123 at 2.5 but not 1 mg kg−1 reduced the pressor responses to ET‐1 in ethanol‐treated rats. Conversely, BQ788 (0.25 mg kg−1) potentiated ET‐1‐induced increases in mean arterial blood pressure in control as well as in ethanol‐treated rats. Interestingly, in the latter group, increases in heart rate, induced by ET‐1 at a dose of 0.025 mg kg−1 were enhanced following ETB receptor blockade. Finally, we observed higher levels of ETA receptor in the heart and mesenteric artery and a reduction of ETB receptor protein levels in the aorta and kidney from rats chronically treated with ethanol.Conclusions and implications:Increased vascular reactivity to ET‐1 and altered protein levels of ETA and ETB receptors could play a role in the pathogenesis of cardiovascular complications associated with chronic ethanol consumption.British Journal of Pharmacology (2008) 154, 971–981; doi:10.1038/bjp.2008.157; published online 12 May 2008

Environmental factors may operate differently when relations are measured across different geographical locations, a phenomenon known as spatial non-stationarity. This study investigates the spatial non-stationarity effect of unhealthy food environments and green spaces on the T2DM prevalence rate at the neighborhood level in Toronto. This study also compares how the results vary between age groups, classified as all adults (20 and above), young adults (from 20 to 44), middle adulthood (from 45 to 64), and seniors (65 and above). The geographically weighted regression model is utilized to explore the impacts of spatial non-stationarity effects on the research results, which may lead to biased conclusions, which have often been ignored in past studies. The results from this study reveal that environmental variables dissimilarly affect T2DM prevalence rates among different age groups and neighborhoods in Toronto after controlling for socioeconomic factors. For example, the green space density yields positive associations with diabetes prevalence rates for elder generations but negative relationships for younger age groups in twenty-two and four neighborhoods, respectively, around Toronto East. The observed associations will provide beneficial suggestions to support government and public health authorities in designing education, prevention, and intervention programs targeting different neighborhoods to control the burden of diabetes.

AbstractBackground and aimsCannabis and alcohol are frequently detected in fatal and injury motor vehicle crashes. While epidemiological meta‐analyses of cannabis and alcohol have found associations with an increase in crash risk, convergent evidence from driving performance measures is insufficiently quantitatively characterized. Our objectives were to quantify the magnitude of the effect of cannabis and alcohol—alone and in combination—on driving performance and behaviour.MethodsSystematic review and meta‐analysis. We systematically searched Academic Search Complete, CINAHL, Embase, Scopus, Google Scholar, MEDLINE, PsycINFO, SPORTDiscus and TRID. Of the 616 studies that underwent full‐text review, this meta‐analysis represents 57 studies and 1725 participants. We extracted data for hazard response time, lateral position variability, lane deviations or excursions, time out of lane, driving speed, driving speed variability, speed violations, time speeding, headway, headway variability and crashes from experimental driving studies (i.e. driving simulator, closed‐course, on‐road) involving cannabis and/or alcohol administration. We reported meta‐analyses of effect sizes using Hedges’ g and r.ResultsCannabis alone was associated with impaired lateral control [e.g. g = 0.331, 95% confidence interval (CI) = 0.212–0.451 for lateral position variability; g = 0.198, 95% CI = 0.001–0.395 for lane excursions) and decreased driving speed (g = –0.176, 95% CI = –0.298 to –0.053]. The combination of cannabis and alcohol was associated with greater driving performance decrements than either drug in isolation [e.g. g = 0.480, 95% CI = 0.096–0.865 for lateral position variability (combination versus alcohol); g = 0.525, 95% CI = 0.049–1.002 for time out of lane (versus alcohol); g = 0.336, 95% CI = 0.036–0.636 for lateral position variability (combination versus cannabis; g = 0.475, 95% CI = 0.002–0.949 for time out of lane (combination versus cannabis)]. Subgroup analyses indicated that the effects of cannabis on driving performance measures were similar to low blood alcohol concentrations. A scarcity of data and study heterogeneity limited the interpretation of some measures.ConclusionsThis meta‐analysis indicates that cannabis, like alcohol, impairs driving, and the combination of the two drugs is more detrimental to driving performance than either in isolation.

AbstractAutotrophs play an essential role in the cycling of carbon and nutrients, yet disease‐ecosystem relationships are often overlooked in these dynamics. Importantly, the availability of elemental nutrients like nitrogen and phosphorus impacts infectious disease in autotrophs, and disease can induce reciprocal effects on ecosystem nutrient dynamics. Relationships linking infectious disease with ecosystem nutrient dynamics are bidirectional, though the interdependence of these processes has received little attention. We introduce disease‐mediated nutrient dynamics (DND) as a framework to describe the multiple, concurrent pathways linking elemental cycles with infectious disease. We illustrate the impact of disease–ecosystem feedback loops on both disease and ecosystem nutrient dynamics using a simple mathematical model, combining approaches from classical ecological (logistic and Droop growth) and epidemiological (susceptible and infected compartments) theory. Our model incorporates the effects of nutrient availability on the growth rates of susceptible and infected autotroph hosts and tracks the return of nutrients to the environment following host death. While focused on autotroph hosts here, the DND framework is generalizable to higher trophic levels. Our results illustrate the surprisingly complex dynamics of host populations, infection patterns, and ecosystem nutrient cycling that can arise from even a relatively simple feedback between disease and nutrients. Feedback loops in disease‐mediated nutrient dynamics arise via effects of infection and nutrient supply on host stoichiometry and population size. Our model illustrates how host growth rate, defense, and tissue chemistry can impact the dynamics of disease–ecosystem relationships. We use the model to motivate a review of empirical examples from autotroph–pathogen systems in aquatic and terrestrial environments, demonstrating the key role of nutrient–disease and disease–nutrient relationships in real systems. By assessing existing evidence and uncovering data gaps and apparent mismatches between model predictions and the dynamics of empirical systems, we highlight priorities for future research intended to narrow the persistent disciplinary gap between disease and ecosystem ecology. Future empirical and theoretical work explicitly examining the dynamic linkages between disease and ecosystem ecology will inform fundamental understanding for each discipline and will better position the field of ecology to predict the dynamics of disease and elemental cycles in the context of global change.

In this work, we investigated the impact of temperature on two-phase transport in low temperature (LT)-polymer electrolyte membrane (PEM) electrolyzer anode flow channels via in operando neutron imaging and observed a decrease in mass transport overpotential with increasing temperature. We observed an increase in anode oxygen gas content with increasing temperature, which was counter-intu.itive to the trends in mass transport overpotential. We attributed this counterintuitive decrease in mass transport overpotential to the enhanced reactant distribution in the flow channels as a result of the temperature increase, determined via a one-dimensional analytical model. We further determined that gas accumulation and fluid property changes are competing, temperature-dependent contributors to mass transport overpotential; however, liquid water viscosity changes led to the dominate enhancement of reactant water distributions in the anode. We present this temperature-dependent mass transport overpotential as a great opportunity for further increasing the voltage efficiency of PEM electrolyzers.

Failure to successfully implement and sustain change over the long term continues to be a major problem in health and social care. Translating evidence into routine clinical practice is notoriously complex, and it is recognised that to implement new evidence-based interventions and sustain them over time, professional behaviour needs to change accordingly. A number of theories and frameworks have been developed to support behaviour change among health and social care professionals, and models of sustainability are emerging, but few have translated into valid and reliable interventions. The long-term success of healthcare professional behavioural change interventions is variable, and the characteristics of successful interventions unclear. Previous reviews have synthesised the evidence for behaviour change, but none have focused on sustainability. In addition, multiple overlapping reviews have reported inconsistent results, which do not aid translation of evidence into practice. Overviews of reviews can provide accessible succinct summaries of evidence and address barriers to evidence-based practice. We aim to compile an overview of reviews, identifying, appraising and synthesising evidence relating to sustained social and healthcare professional behaviour change.We will conduct a systematic review of Cochrane reviews (an Overview). We plan to systematically search the Cochrane Database of Systematic Reviews. We will include all systematic reviews of randomised controlled trials comparing a healthcare professional targeted behaviour change intervention to a standard care or no intervention control group. Two reviewers will independently assess the eligibility of the reviews and the methodological quality of included reviews using the ROBIS tool. The quality of evidence within each comparison in each review will be judged based on the GRADE criteria. Disagreements will be resolved through discussion. Effects of interventions will be systematically tabulated and the quality of evidence used to determine implications for clinical practice and make recommendations for future research.This overview will bring together the best available evidence relating to the sustainability of health professional behaviour change, thus supporting policy makers with decision-making in this field.