Fuel poverty increases risk of mould contamination, regardless of adult risk perception & ventilation in social housing properties

INTRODUCTION: Fuel poverty affects 2.4 million UK homes leading to poor hygrothermal conditions and risk of mould and house dust mite contaminations, which in turn increases risk of asthma exacerbation. For the first time we assess how fuel poverty, occupants' risk perception and use of mechanical ventilation mediate the risk of mould contamination in social housing. METHODS: Postal questionnaires were sent to 3867 social housing properties to collect adult risk perception, and demographic and environmental information on occupants. Participant details were linked to data pertaining to the individual properties. Multiple logistic regression was used to calculate odds ratios and confidence intervals while allowing for clustering of individuals coming from the same housing estate. We used Structured Equation Modelling and Goodness of Fit analysis in mediation analyses to examine the role of fuel poverty, risk perception, use of ventilation and energy efficiency. RESULTS: Eighteen percent of our target social housing populations (671 households) were included into our study. High risk perception (score of 8-10) was associated with reduced risk of mould contamination in the bedrooms of children (OR 0.5 95% CI; 0.3-0.9) and adults (OR 0.4 95% CI; 0.3-0.7). High risk perception of living with inadequate heating and ventilation reduced the risk of mould contamination (OR 0.5 95% CI; 0.3-0.8 and OR 0.5 95% CI; 0.3-0.7, respectively). Participants living with inadequate heating and not heating due to the cost of fuel had an increased risk of mould contamination (OR 3.4 95% CI; 2.0-5.8 and OR 2.2 95% CI; 1.5-3.2, respectively). Increased risk perception and use of extractor fans did not mediate the association between fuel poverty behaviours and increased risk of mould contamination. DISCUSSION: Fuel poverty behaviours increased the risk of mould contamination, which corresponds with existing literature. For the first time we used mediation analysis to assess how this association maybe modified by occupant behaviours. Increased risk perception and use of extractor fans did not modify the association between fuel poverty and mould contamination. This suggests that fuel poor populations may not benefit from energy efficiency interventions due to ineffective heating and ventilation practices of those occupants residing participating households. Our findings may be modified by a complex interaction between occupant behaviours and the built environment. We found that participant age, occupancy, SES, pets, drying washing indoors, geographic location, architectural design/age of the property, levels of insulation and type of heating regulated risk of mould contamination. CONCLUSION: Fuel poverty behaviours affected around a third of participating households and represent a risk factor for increased exposures to damp and mouldy conditions, regardless of adult risk perception, heating and ventilation practices. This requires multidisciplinary approach to assess the complex interaction between occupant behaviours, risk perception, the built environment and the effective use of heating and ventilation practices. STUDY IMPLICATIONS: Our findings have implications for housing policies and future housing interventions. Effective communication strategies focusing on awareness and perception of risk may help address indoor air quality issues. This must be supported by improved household energy efficiency with the provision of more effective heating and ventilation strategies, specifically to help alleviate those suffering from fuel poverty.European Regional Development Fund Programme  202497 50002

Targeted disruption of melanin biosynthesis genes in the human pathogenic fungus Lomentospora prolificans and its consequences for pathogen survival

PublishedArticleThe dematiaceous (melanised) fungus Lomentospora (Scedosporium) prolificans is a life-threatening opportunistic pathogen of immunocompromised humans, resistant to anti-fungal drugs. Melanin has been shown to protect human pathogenic fungi against antifungal drugs, oxidative killing and environmental stresses. To determine the protective role of melanin in L. prolificans to oxidative killing (H2O2), UV radiation and the polyene anti-fungal drug amphotericin B, targeted gene disruption was used to generate mutants of the pathogen lacking the dihydroxynaphthalene (DHN)-melanin biosynthetic enzymes polyketide synthase (PKS1), tetrahydroxynapthalene reductase (4HNR) and scytalone dehydratase (SCD1). Infectious propagules (spores) of the wild-type strain 3.1 were black/brown, whereas spores of the PKS-deficient mutant ΔLppks1::hph were white. Complementation of the albino mutant ΔLppks1::hph restored the black-brown spore pigmentation, while the 4HNR-deficient mutant ΔLp4hnr::hph and SCD-deficient mutant ΔLpscd1::hph both produced orange-yellow spores. The mutants ΔLppks1::hph and ΔLp4hnr::hph showed significant reductions in spore survival following H2O2 treatment, while spores of ΔLpscd1::hph and the ΔLppks1::hph complemented strain ΔLppks1::hph:PKS showed spore survivals similar to strain 3.1. Spores of the mutants ΔLp4hnr::hph and ΔLpscd1::hph and complemented strain ΔLppks1::hph:PKS showed spore survivals similar to 3.1 following exposure to UV radiation, but survival of ΔLppks1::hph spores was significantly reduced compared to the wild-type strain. Strain 3.1 and mutants ΔLp4hnr::hph and ΔLppks1::hph:PKS were resistant to amphotericin B while, paradoxically, the PKS1- and SCD1-deficient mutants showed significant increases in growth in the presence of the antifungal drug. Taken together, these results show that while melanin plays a protective role in the survival of the pathogen to oxidative killing and UV radiation, melanin does not contribute to its resistance to amphotericin B

Long-haul northeast travel disrupts sleep and induces perceived fatigue in endurance athletes

Introduction: Long-haul transmeridian travel is known to cause disruptions to sleep and immune status, which may increase the risk of illness. Aim: This study aimed to determine the effects of long-haul northeast travel for competition on sleep, illness and preparedness in endurance athletes. Methods: Twelve trained (13.8 ± 3.2 training h/week) masters (age: 48 ± 14 years) triathletes were monitored for sleep (quantity via actigraphy and quality via self-report), mucosal immunity (salivary immunoglobulin-A) and stress (salivary cortisol) as well as self-reported illness, fatigue, recovery and preparedness. Baseline measures were recorded for 2 weeks prior to travel for all variables except for the saliva samples, which were collected on three separate days upon waking. Participants completed normal training during the baseline period. Measures were subsequently recorded before, during and after long-haul northeast travel from the Australian winter to the Hawaiian summer, and in the lead up to an Ironman 70.3 triathlon. Results: All comparisons are to baseline. There was a most likely decrease in sleep duration on the over-night flight (-4.8 ± 1.2 h; effect size; ±90% confidence limits = 3.06; ±1.26) and a very likely increase in sleep duration on the first night after arrival (0.7 ± 1.0 h; 1.15; ±0.92). After this time, sleep duration returned to baseline for several days until it was very likely decreased on the night prior to competition (-1.2 ± 1.0 h; 1.18; ±0.93). Nap duration was likely increased on the first day after arrival (36 ± 65 min; 3.90; ±3.70). There was also a likely increase in self-reported fatigue upon waking after the first night in the new destination (1.1 ± 1.6 AU; 0.54; ±0.41) and there were three athletes (25%) who developed symptoms of illness 3-5 days after arrival. There were no changes in sleep quality or mucosal measures across study. Discussion: Long-haul northeast travel from a cool to a hot environment had substantial influences on sleep and self-reported fatigue, but these alterations had returned to pre-departure baseline 48 h after arrival. Endurance athletes undertaking similar journeys may benefit from optimizing sleep hygiene, especially on the first 2 days after arrival, or until sleep duration and fatigue levels return to normal

Long-Haul Northeast Travel Disrupts Sleep and Induces Perceived Fatigue in Endurance Athletes

Introduction: Long-haul transmeridian travel is known to cause disruptions to sleep and immune status, which may increase the risk of illness.Aim: This study aimed to determine the effects of long-haul northeast travel for competition on sleep, illness and preparedness in endurance athletes.Methods: Twelve trained (13.8 ± 3.2 training h/week) masters (age: 48 ± 14 years) triathletes were monitored for sleep (quantity via actigraphy and quality via self-report), mucosal immunity (salivary immunoglobulin-A) and stress (salivary cortisol) as well as self-reported illness, fatigue, recovery and preparedness. Baseline measures were recorded for 2 weeks prior to travel for all variables except for the saliva samples, which were collected on three separate days upon waking. Participants completed normal training during the baseline period. Measures were subsequently recorded before, during and after long-haul northeast travel from the Australian winter to the Hawaiian summer, and in the lead up to an Ironman 70.3 triathlon.Results: All comparisons are to baseline. There was a most likely decrease in sleep duration on the over-night flight (-4.8 ± 1.2 h; effect size; ±90% confidence limits = 3.06; ±1.26) and a very likely increase in sleep duration on the first night after arrival (0.7 ± 1.0 h; 1.15; ±0.92). After this time, sleep duration returned to baseline for several days until it was very likely decreased on the night prior to competition (-1.2 ± 1.0 h; 1.18; ±0.93). Nap duration was likely increased on the first day after arrival (36 ± 65 min; 3.90; ±3.70). There was also a likely increase in self-reported fatigue upon waking after the first night in the new destination (1.1 ± 1.6 AU; 0.54; ±0.41) and there were three athletes (25%) who developed symptoms of illness 3–5 days after arrival. There were no changes in sleep quality or mucosal measures across study.Discussion: Long-haul northeast travel from a cool to a hot environment had substantial influences on sleep and self-reported fatigue, but these alterations had returned to pre-departure baseline 48 h after arrival. Endurance athletes undertaking similar journeys may benefit from optimizing sleep hygiene, especially on the first 2 days after arrival, or until sleep duration and fatigue levels return to normal

RNA interference of endochitinases in the sugarcane endophyte Trichoderma virens 223 reduces its fitness as a biocontrol agent of pineapple disease

publication-status: PublishedThe sugarcane root endophyte Trichoderma virens 223 holds enormous potential as a sustainable alternative to chemical pesticides in the control of sugarcane diseases. Its efficacy as a biocontrol agent is thought to be associated with its production of chitinase enzymes, including N-acetyl-β-D-glucosaminidases, chitobiosidases and endochitinases. We used targeted gene deletion and RNA-dependent gene silencing strategies to disrupt N-acetyl-β-D-glucosaminidase and endochitinase activities of the fungus, and to determine their roles in the biocontrol of soil-borne plant pathogens. The loss of N-acetyl-β-D-glucosaminidase activities was dispensable for biocontrol of the plurivorous damping-off pathogens Rhizoctonia solani and Sclerotinia sclerotiorum, and of the sugarcane pathogen Ceratocystis paradoxa, the causal agent of pineapple disease. Similarly, suppression of endochitinase activities had no effect on R. solani and S. sclerotiorum disease control, but had a pronounced effect on the ability of T. virens 223 to control pineapple disease. Our work demonstrates a critical requirement for T. virens 223 endochitinase activity in the biocontrol of C. paradoxa sugarcane disease, but not for general antagonism of other soil pathogens. This may reflect its lifestyle as a sugarcane root endophyte

Quantification of habitat fragmentation reveals extinction risk in terrestrial mammals

Although habitat fragmentation is often assumed to be a primary driver of extinction, global patterns of fragmentation and its relationship to extinction risk have not been consistently quantified for any major animal taxon. We developed high-resolution habitat fragmentation models and used phylogenetic comparative methods to quantify the effects of habitat fragmentation on the world's terrestrial mammals, including 4,018 species across 26 taxonomic Orders. Results demonstrate that species with more fragmentation are at greater risk of extinction, even after accounting for the effects of key macroecological predictors, such as body size and geographic range size. Species with higher fragmentation had smaller ranges and a lower proportion of high-suitability habitat within their range, andmost high-suitability habitat occurred outside of protected areas, further elevating extinction risk. Our models provide a quantitative evaluation of extinction risk assessments for species, allow for identification of emerging threats in species not classified as threatened, and provide maps of global hotspots of fragmentation for the world's terrestrial mammals. Quantification of habitat fragmentation will help guide threat assessment and strategic priorities for global mammal conservation

Transcriptional reprogramming underpins enhanced plant growth promotion by the biocontrol fungus Trichoderma hamatum GD12 during antagonistic interactions with Sclerotinia sclerotiorumin soil

The free-living soil fungus Trichoderma hamatum strain GD12 is notable amongst Trichoderma strains in both controlling plant diseases and in stimulating plant growth, a property enhanced during its antagonistic interactions with pathogens in soil. These attributes, alongside its markedly expanded genome and proteome compared to other biocontrol and plant growth promoting Trichoderma strains, imply a rich potential for sustainable alternatives to synthetic pesticides and fertilisers for controlling plant disease and increasing yields. The purpose of this study was to investigate the transcriptional responses of GD12 underpinning its biocontrol and plant growth promotion capabilities during antagonistic interactions with the pathogen Sclerotinia sclerotiorum in soil. Using an extensive mRNA-seq study capturing different time points during the pathogen-antagonist interaction in soil, we show that dynamic and biphasic signatures in the GD12 transcriptome underpin its biocontrol and plant (lettuce) growth promotional activities. Functional predictions of differentially expressed genes demonstrate the enrichment of transcripts encoding proteins involved in transportation and oxidation-reduction reactions during both processes and an over-representation of siderophores. We identify a biphasic response during biocontrol characterised by a significant induction of transcripts encoding small-secreted cysteine rich proteins, secondary metabolite producing gene clusters and genes unique to GD12. These data support the hypothesis that Sclerotinia biocontrol is mediated by the synthesis and secretion of antifungal compounds and that GD12's unique reservoir of uncharacterised genes is actively recruited during effective biological control of a plurivorous plant pathogen. This article is protected by copyright. All rights reserved

Pre-clinical imaging of invasive candidiasis using ImmunoPET/MR

This is the final version of the article. Available from Frontiers Media via the DOI in this record.The human commensal yeast Candida is the 4th most common cause of hospital-acquired bloodstream infections, with C. albicans accounting for the majority of the >400,000 life-threatening infections annually. Diagnosis of invasive candidiasis (IC), a disease encompassing candidemia (blood-borne yeast infection) and deep-seated organ infections, is a major challenge since clinical manifestations of the disease are indistinguishable from viral, bacterial and other fungal diseases, and diagnostic tests for biomarkers in the bloodstream such as PCR, ELISA and pan-fungal β-D-glucan lack either standardisation, sensitivity or specificity. Blood culture remains the gold standard for diagnosis, but test sensitivity is poor and turn-around time slow. Furthermore, cultures can only be obtained when the yeast resides in the bloodstream, with samples recovered from hematogenous infections often yielding negative results. Consequently, there is a pressing need for a diagnostic test that allows the identification of metastatic foci in deep-seated Candida infections, without the need for invasive biopsy. Here, we report the development of a highly specific mouse IgG3 monoclonal antibody (MC3) that binds to a putative β-1,2-mannan epitope present in high molecular weight mannoproteins and phospholipomannans on the surface of yeast and hyphal morphotypes of C. albicans, and its use as a [64Cu]NODAGA-labeled tracer for whole-body pre-clinical imaging of deep-seated C. albicans infections using antibody-guided positron emission tomography and magnetic resonance imaging (immunoPET/MRI). When used in a mouse intravenous (i.v.) challenge model that faithfully mimics disseminated C. albicans infections in humans, the [64Cu]NODAGA-MC3 tracer accurately detects infections of the kidney, the principal site of blood-borne candidiasis. Using a strain of the emerging human pathogen Candida auris that reacts with MC3 in vitro, but which is non-infective in i.v. challenged mice, we demonstrate the accuracy of the tracer in diagnosing invasive infections in vivo. This pre-clinical study demonstrates the principle of antibody-guided molecular imaging for detection of deep organ infections in IC, without the need for invasive tissue biopsy.This work was supported, in part, by the European Union Seventh Framework Program FP7/2007-2013 under grant 602820

Performance of lateral flow device and galactomannan for the detection of Aspergillus species in bronchoalveolar fluid of patients at risk for invasive pulmonary aspergillosis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111755/1/myc12327.pd

Social and Structural Factors Associated With Substance Use within the Support Network of Adults Living In Precarious Housing in A Socially Marginalized Neighborhood of Vancouver, Canada

Background The structure of a social network as well as peer behaviours are thought to affect personal substance use. Where substance use may create health risks, understanding the contribution of social networks to substance use may be valuable for the design and implementation of harm reduction or other interventions. We examined the social support network of people living in precarious housing in a socially marginalized neighborhood of Vancouver, and analysed associations between social network structure, personal substance use, and supporters’ substance use. Methods An ongoing, longitudinal study recruited 246 participants from four single room occupancy hotels, with 201 providing social network information aligned with a 6-month observation period. Use of tobacco, alcohol, cannabis, cocaine (crack and powder), methamphetamine, and heroin was recorded at monthly visits. Ego- and graph-level measures were calculated; the dispersion and prevalence of substances in the network was described. Logistic mixed effects models were used to estimate the association between ego substance use and peer substance use. Permutation analysis was done to test for randomness of substance use dispersion on the social network. Results The network topology corresponded to residence (Hotel) with two clusters differing in demographic characteristics (Cluster 1 –Hotel A: 94% of members, Cluster 2 –Hotel B: 95% of members). Dispersion of substance use across the network demonstrated differences according to network topology and specific substance. Methamphetamine use (overall 12%) was almost entirely limited to Cluster 1, and absent from Cluster 2. Different patterns were observed for other substances. Overall, ego substance use did not differ over the six-month period of observation. Ego heroin, cannabis, or crack cocaine use was associated with alter use of the same substances. Ego methamphetamine, powder cocaine, or alcohol use was not associated with alter use, with the exception for methamphetamine in a densely using part of the network. For alters using multiple substances, cannabis use was associated with lower ego heroin use, and lower ego crack cocaine use. Permutation analysis also provided evidence that dispersion of substance use, and the association between ego and alter use was not random for all substances. Conclusions In a socially marginalized neighborhood, social network topology was strongly influenced by residence, and in turn was associated with type(s) of substance use. Associations between personal use and supporter’s use of a substance differed across substances. These complex associations may merit consideration in the design of interventions to reduce risk and harms associated with substance use in people living in precarious housing