108 research outputs found

    Aircraft-Engine Particulate Matter Emissions from Conventional and Sustainable Aviation Fuel Combustion: Comparison of Measurement Techniques for Mass, Number, and Size

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    Sustainable aviation fuels (SAFs) have different compositions compared to conventional petroleum jet fuels, particularly in terms of fuel sulfur and hydrocarbon content. These differences may change the amount and physicochemical properties of volatile and non-volatile particulate matter (nvPM) emitted by aircraft engines. In this study, we evaluate whether comparable nvPM measurement techniques respond similarly to nvPM produced by three blends of SAFs compared to three conventional fuels. Multiple SAF blends and conventional (Jet A-1) jet fuels were combusted in a V2527-A5 engine, while an additional conventional fuel (JP-8) was combusted in a CFM56-2C1 engine. We evaluated nvPM mass concentration measured by three real-Time measurement techniques: photoacoustic spectroscopy, laser-induced incandescence, and the extinction-minus-scattering technique. Various commercial instruments were tested, including three laser-induced incandescence (LII) 300s, one photoacoustic extinctiometer (PAX), one micro soot sensor (MSS+), and two cavity-Attenuated phase shift PMSSA (CAPS PMSSA) instruments. Mass-based emission indices (EIm) reported by these techniques were similar, falling within 30ĝ€¯% of their geometric mean for EIm above 100ĝ€¯mg per kg fuel (approximately 10ĝ€¯μgĝ€¯PMĝ€¯m-3 at the instrument); this geometric mean was therefore used as a reference value. Additionally, two integrative measurement techniques were evaluated: filter photometry and particle size distribution (PSD) integration. The commercial instruments used were one tricolor absorption photometer (TAP), one particle soot absorption photometer (PSAP), and two scanning mobility particle sizers (SMPSs). The TAP and PSAP were operated at 5ĝ€¯% and 10ĝ€¯% of their nominal flow rates, respectively, to extend the life of their filters. These techniques are used in specific applications, such as on board research aircraft to determine particulate matter (PM) emissions at cruise. EIm reported by the alternative techniques fell within approximately 50ĝ€¯% of the mean aerosol-phase EIm. In addition, we measured PM-number-based emission indices using PSDs and condensation particle counters (CPCs). The commercial instruments used included TSI SMPSs, a Cambustion differential mobility spectrometer (DMS500), and an AVL particle counter (APC), and the data also fell within approximately 50ĝ€¯% of their geometric mean. The number-based emission indices were highly sensitive to the accuracy of the sampling-line penetration functions applied as corrections. In contrast, the EIm data were less sensitive to those corrections since a smaller volume fraction fell within the size range where corrections were substantial. A separate, dedicated experiment also showed that the operating laser fluence used in the LII 300 laser-induced incandescence instrument for aircraft-engine nvPM measurement is adequate for a range of SAF blends investigated in this study. Overall, we conclude that all tested instruments are suitable for the measurement of nvPM emissions from the combustion of SAF blends in aircraft engines

    Clinical Relevance and Discriminatory Value of Elevated Liver Aminotransferase Levels for Dengue Severity

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    Dengue is a global public health problem, as the incidence of the disease has reached hyperendemic proportions in recent decades. Infection with dengue can cause acute, febrile illness or severe disease, which can lead to plasma leakage, bleeding, and organ impairment. One of the most prominent clinical characteristics of dengue patients is increased aspartate and alanine aminotransferase liver enzyme levels. The significance of this is uncertain, as it is transient in the majority of cases, and most patients recover uneventfully without liver damage. In this study, we characterized this phenomenon in the context of dengue severity and found that, although liver enzyme levels increased concurrently with dengue severity, they could not sufficiently discriminate between dengue fever and dengue hemorrhagic fever or between non-severe and severe dengue. Therefore clinicians may need to use other parameters to distinguish dengue severity in patients during early illness

    Diabetes with Hypertension as Risk Factors for Adult Dengue Hemorrhagic Fever in a Predominantly Dengue Serotype 2 Epidemic: A Case Control Study

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    Dengue is a major vector borne disease in the tropical and subtropical regions. An estimated 50 million infections occur per annum in over 100 countries. A severe form of dengue, characterized by bleeding and plasma leakage, known as dengue hemorrhagic fever (DHF) is estimated to occur in 1–5% of hospitalized cases. It can be fatal if unrecognized and not treated in a timely manner. Previous studies had found a number of risk factors for DHF. However, screening and clinical management strategies based on these risk factors may not be applicable to all populations and epidemics of different serotypes. In this study, we found significant association between DHF and diabetes mellitus and diabetes mellitus with hypertension during the epidemic of predominantly serotype 2 (year 2007 and 2008), but not during the epidemic of predominantly serotype 1 (year 2006). Diabetes mellitus and hypertension are prevalent in Singapore and most parts of South-East Asia, where dengue is endemic. Therefore, it is important to address the risk effect of these co-morbidities on the development of DHF so as to reduce morbidity and mortality. Our findings may have impact on screening and clinical management of dengue patients, when confirmed in more studies

    MRSA transmission dynamics among interconnected acute, intermediate-term, and long-term healthcare facilities in Singapore

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    This work was supported by the Ministry of Health, Singapore (Communicable Diseases–Public Health Research Grant), the Wellcome Trust (Institutional Strategic Support Fund award [grant 097831/Z/11/Z] to the University of St Andrews Bioinformatics Unit), and the Scottish Infection Research Network and Chief Scientist Office (Scottish Healthcare Associated Infection Prevention Institute consortium funding [Chief Scientist Office reference SIRN10] to K. P. and M. T. G. H.).Background: Methicillin-resistant Staphylococcus aureus (MRSA) is the most common healthcare-associated multidrug-resistant organism. Despite the interconnectedness between acute care hospitals (ACHs) and intermediate- and long-term care facilities (ILTCFs), the transmission dynamics of MRSA between healthcare settings is not well understood. Methods: We conducted a cross-sectional study in a network comprising an ACH and 5 closely affiliated ILTCFs in Singapore. A total of 1700 inpatients were screened for MRSA over a 6-week period in 2014. MRSA isolates underwent whole-genome sequencing, with a pairwise single-nucleotide polymorphism (Hamming distance) cutoff of 60 core genome single-nucleotide polymorphisms used to define recent transmission clusters (clades) for the 3 major clones. Results: MRSA prevalence was significantly higher in intermediate-term (29.9%) and long-term (20.4%) care facilities than in the ACH (11.8%) (P < .001). The predominant clones were sequence type [ST] 22 (n = 183; 47.8%), ST45 (n = 129; 33.7%), and ST239 (n = 26; 6.8%), with greater diversity of STs in ILTCFs relative to the ACH. A large proportion of the clades in ST22 (14 of 21 clades; 67%) and ST45 (7 of 13; 54%) included inpatients from the ACH and ILTCFs. The most frequent source of the interfacility transmissions was the ACH (n = 28 transmission events; 36.4%). Conclusions: MRSA transmission dynamics between the ACH and ILTCFs were complex. The greater diversity of STs in ILTCFs suggests that the ecosystem in such settings might be more conducive for intrafacility transmission events. ST22 and ST45 have successfully established themselves in ILTCFs. The importance of interconnected infection prevention and control measures and strategies cannot be overemphasized.PostprintPeer reviewe

    All Our Babies Cohort Study: recruitment of a cohort to predict women at risk of preterm birth through the examination of gene expression profiles and the environment

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    <p>Abstract</p> <p>Background</p> <p>Preterm birth is the leading cause of perinatal morbidity and mortality. Risk factors for preterm birth include a personal or familial history of preterm delivery, ethnicity and low socioeconomic status yet the ability to predict preterm delivery before the onset of preterm labour evades clinical practice. Evidence suggests that genetics may play a role in the multi-factorial pathophysiology of preterm birth. The All Our Babies Study is an on-going community based longitudinal cohort study that was designed to establish a cohort of women to investigate how a women's genetics and environment contribute to the pathophysiology of preterm birth. Specifically this study will examine the predictive potential of maternal leukocytes for predicting preterm birth in non-labouring women through the examination of gene expression profiles and gene-environment interactions.</p> <p>Methods/Design</p> <p>Collaborations have been established between clinical lab services, the provincial health service provider and researchers to create an interdisciplinary study design for the All Our Babies Study. A birth cohort of 2000 women has been established to address this research question. Women provide informed consent for blood sample collection, linkage to medical records and complete questionnaires related to prenatal health, service utilization, social support, emotional and physical health, demographics, and breast and infant feeding. Maternal blood samples are collected in PAXgene™ RNA tubes between 18-22 and 28-32 weeks gestation for transcriptomic analyses.</p> <p>Discussion</p> <p>The All Our Babies Study is an example of how investment in clinical-academic-community partnerships can improve research efficiency and accelerate the recruitment and data collection phases of a study. Establishing these partnerships during the study design phase and maintaining these relationships through the duration of the study provides the unique opportunity to investigate the multi-causal factors of preterm birth. The overall All Our Babies Study results can potentially lead to healthier pregnancies, mothers, infants and children.</p

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Determinants of recovery from post-COVID-19 dyspnoea: analysis of UK prospective cohorts of hospitalised COVID-19 patients and community-based controls

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    Background The risk factors for recovery from COVID-19 dyspnoea are poorly understood. We investigated determinants of recovery from dyspnoea in adults with COVID-19 and compared these to determinants of recovery from non-COVID-19 dyspnoea. Methods We used data from two prospective cohort studies: PHOSP-COVID (patients hospitalised between March 2020 and April 2021 with COVID-19) and COVIDENCE UK (community cohort studied over the same time period). PHOSP-COVID data were collected during hospitalisation and at 5-month and 1-year follow-up visits. COVIDENCE UK data were obtained through baseline and monthly online questionnaires. Dyspnoea was measured in both cohorts with the Medical Research Council Dyspnoea Scale. We used multivariable logistic regression to identify determinants associated with a reduction in dyspnoea between 5-month and 1-year follow-up. Findings We included 990 PHOSP-COVID and 3309 COVIDENCE UK participants. We observed higher odds of improvement between 5-month and 1-year follow-up among PHOSP-COVID participants who were younger (odds ratio 1.02 per year, 95% CI 1.01–1.03), male (1.54, 1.16–2.04), neither obese nor severely obese (1.82, 1.06–3.13 and 4.19, 2.14–8.19, respectively), had no pre-existing anxiety or depression (1.56, 1.09–2.22) or cardiovascular disease (1.33, 1.00–1.79), and shorter hospital admission (1.01 per day, 1.00–1.02). Similar associations were found in those recovering from non-COVID-19 dyspnoea, excluding age (and length of hospital admission). Interpretation Factors associated with dyspnoea recovery at 1-year post-discharge among patients hospitalised with COVID-19 were similar to those among community controls without COVID-19. Funding PHOSP-COVID is supported by a grant from the MRC-UK Research and Innovation and the Department of Health and Social Care through the National Institute for Health Research (NIHR) rapid response panel to tackle COVID-19. The views expressed in the publication are those of the author(s) and not necessarily those of the National Health Service (NHS), the NIHR or the Department of Health and Social Care. COVIDENCE UK is supported by the UK Research and Innovation, the National Institute for Health Research, and Barts Charity. The views expressed are those of the authors and not necessarily those of the funders

    Cohort Profile: Post-Hospitalisation COVID-19 (PHOSP-COVID) study

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    Hair Cortisol in Twins : Heritability and Genetic Overlap with Psychological Variables and Stress-System Genes

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    A. Palotie on työryhmän jäsen.Hair cortisol concentration (HCC) is a promising measure of long-term hypothalamus-pituitary-adrenal (HPA) axis activity. Previous research has suggested an association between HCC and psychological variables, and initial studies of inter-individual variance in HCC have implicated genetic factors. However, whether HCC and psychological variables share genetic risk factors remains unclear. The aims of the present twin study were to: (i) assess the heritability of HCC; (ii) estimate the phenotypic and genetic correlation between HPA axis activity and the psychological variables perceived stress, depressive symptoms, and neuroticism; using formal genetic twin models and molecular genetic methods, i.e. polygenic risk scores (PRS). HCC was measured in 671 adolescents and young adults. These included 115 monozygotic and 183 dizygotic twin-pairs. For 432 subjects PRS scores for plasma cortisol, major depression, and neuroticism were calculated using data from large genome wide association studies. The twin model revealed a heritability for HCC of 72%. No significant phenotypic or genetic correlation was found between HCC and the three psychological variables of interest. PRS did not explain variance in HCC. The present data suggest that HCC is highly heritable. However, the data do not support a strong biological link between HCC and any of the investigated psychological variables.Peer reviewe
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