Whole-genome characterization of a Shewanella algae strain coharboring blaCTX-M-15 and armA genes on a novel IncC plasmid

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Seasonal patterns of outdoor PM infiltration into indoor environments: review and meta-analysis of available studies from different climatological zones in Europe

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Short-term joint effects of PM10, NO2 and SO2 on cardio-respiratory disease hospital admissions in Cape Town, South Africa

BACKGROUND/AIM : In sub-Sahara Africa, few studies have investigated the short-term association between hospital admissions and ambient air pollution. Therefore, this study explored the association between multiple air pollutants and hospital admissions in Cape Town, South Africa. METHODS : Generalized additive quasi-Poisson models were used within a distributed lag linear modelling framework to estimate the cumulative effects of PM10, NO2 , and SO2 up to a lag of 21 days. We further conducted multi-pollutant models and stratified our analysis by age group, sex, and season. RESULTS : The overall relative risk (95% confidence interval (CI)) for PM10, NO2 , and SO2 at lag 0–1 for hospital admissions due to respiratory disease (RD) were 1.9% (0.5–3.2%), 2.3% (0.6–4%), and 1.1% (−0.2–2.4%), respectively. For cardiovascular disease (CVD), these values were 2.1% (0.6–3.5%), 1% (−0.8–2.8%), and −0.3% (−1.6–1.1%), respectively, per inter-quartile range increase of 12 µg/m3 for PM10, 7.3 µg/m3 for NO2 , and 3.6 µg/m3 for SO2 . The overall cumulative risks for RD per IQR increase in PM10 and NO2 for children were 2% (0.2–3.9%) and 3.1% (0.7–5.6%), respectively. CONCLUSION : We found robust associations of daily respiratory disease hospital admissions with daily PM10 and NO2 concentrations. Associations were strongest among children and warm season for RD.DATA AVAILABILITY STATEMENT : Exposure data are available for download on the South African Air Quality Information System (SAAQIS) https://saaqis.environment.gov.za/; (accessed on 22 April 2019) however, restrictions apply to the health outcome data.SUPPLEMENTARY MATERIAL : This document describes the air pollution data by station for each year and outlines the imputation analysis. In addition, it tabulates the estimates for age groups, sex, and season per interquartile range and 10 µg/m3.https://www.mdpi.com/journal/ijerphSchool of Health Systems and Public Health (SHSPH

Simulation of population-based commuter exposure to NO2 using different air pollution models

We simulated commuter routes and long-term exposure to traffic-related air pollution during commute in a representative population sample in Basel (Switzerland), and evaluated three air pollution models with different spatial resolution for estimating commute exposures to nitrogen dioxide (NO2) as a marker of long-term exposure to traffic-related air pollution. Our approach includes spatially and temporally resolved data on actual commuter routes, travel modes and three air pollution models. Annual mean NO2 commuter exposures were similar between models. However, we found more within-city and within-subject variability in annual mean (±SD) NO2 commuter exposure with a high resolution dispersion model (40 ± 7 µg m−3, range: 21–61) than with a dispersion model with a lower resolution (39 ± 5 µg m−3; range: 24–51), and a land use regression model (41 ± 5 µg m−3; range: 24–54). Highest median cumulative exposures were calculated along motorized transport and bicycle routes, and the lowest for walking. For estimating commuter exposure within a city and being interested also in small-scale variability between roads, a model with a high resolution is recommended. For larger scale epidemiological health assessment studies, models with a coarser spatial resolution are likely sufficient, especially when study areas include suburban and rural areas

Downregulation of peroxisome proliferator-activated receptors (PPARs) in nasal polyposis

BACKGROUND: Peroxisome proliferator-activated receptor (PPAR) α, βδ and γ are nuclear receptors activated by fatty acid metabolites. An anti-inflammatory role for these receptors in airway inflammation has been suggested. METHODS: Nasal biopsies were obtained from 10 healthy volunteers and 10 patients with symptomatic allergic rhinitis. Nasal polyps were obtained from 22 patients, before and after 4 weeks of local steroid treatment (fluticasone). Real-time RT-PCR was used for mRNA quantification and immunohistochemistry for protein localization and quantification. RESULTS: mRNA expression of PPARα, PPARβδ, PPARγ was found in all specimens. No differences in the expression of PPARs were obtained in nasal biopsies from patients with allergic rhinitis and healthy volunteers. Nasal polyps exhibited lower levels of PPARα and PPARγ than normal nasal mucosa and these levels were, for PPARγ, further reduced following steroid treatment. PPARγ immunoreactivity was detected in the epithelium, but also found in smooth muscle of blood vessels, glandular acini and inflammatory cells. Quantitative evaluation of the epithelial immunostaining revealed no differences between nasal biopsies from patients with allergic rhinitis and healthy volunteers. In polyps, the PPARγ immunoreactivity was lower than in nasal mucosa and further decreased after steroid treatment. CONCLUSION: The down-regulation of PPARγ, in nasal polyposis but not in turbinates during symptomatic seasonal rhinitis, suggests that PPARγ might be of importance in long standing inflammations

Expression of Stretch-Activated Two-Pore Potassium Channels in Human Myometrium in Pregnancy and Labor

Background: We tested the hypothesis that the stretch-activated, four-transmembrane domain, two pore potassium channels (K2P), TREK-1 and TRAAK are gestationally-regulated in human myometrium and contribute to uterine relaxation during pregnancy until labor. Methodology: We determined the gene and protein expression of K2P channels in non-pregnant, pregnant term and preterm laboring myometrium. We employed both molecular biological and functional studies of K2P channels in myometrial samples taken from women undergoing cesarean delivery of a fetus. Principal Findings: TREK-1, but not TREK-2, channels are expressed in human myometrium and significantly up-regulated during pregnancy. Down-regulation of TREK-1 message was seen by Q-PCR in laboring tissues consistent with a role for TREK-1 in maintaining uterine quiescence prior to labor. The TRAAK channel was unregulated in the same women. Blockade of stretch-activated channels with a channel non-specific tarantula toxin (GsMTx-4) or the more specific TREK-1 antagonist L-methionine ethyl ester altered contractile frequency in a dose-dependent manner in pregnant myometrium. Arachidonic acid treatment lowered contractile tension an effect blocked by fluphenazine. Functional studies are consistent with a role for TREK-1 in uterine quiescence. Conclusions: We provide evidence supporting a role for TREK-1 in contributing to uterine quiescence during gestation an

Computational Identification of Transcriptional Regulators in Human Endotoxemia

One of the great challenges in the post-genomic era is to decipher the underlying principles governing the dynamics of biological responses. As modulating gene expression levels is among the key regulatory responses of an organism to changes in its environment, identifying biologically relevant transcriptional regulators and their putative regulatory interactions with target genes is an essential step towards studying the complex dynamics of transcriptional regulation. We present an analysis that integrates various computational and biological aspects to explore the transcriptional regulation of systemic inflammatory responses through a human endotoxemia model. Given a high-dimensional transcriptional profiling dataset from human blood leukocytes, an elementary set of temporal dynamic responses which capture the essence of a pro-inflammatory phase, a counter-regulatory response and a dysregulation in leukocyte bioenergetics has been extracted. Upon identification of these expression patterns, fourteen inflammation-specific gene batteries that represent groups of hypothetically ‘coregulated’ genes are proposed. Subsequently, statistically significant cis-regulatory modules (CRMs) are identified and decomposed into a list of critical transcription factors (34) that are validated largely on primary literature. Finally, our analysis further allows for the construction of a dynamic representation of the temporal transcriptional regulatory program across the host, deciphering possible combinatorial interactions among factors under which they might be active. Although much remains to be explored, this study has computationally identified key transcription factors and proposed a putative time-dependent transcriptional regulatory program associated with critical transcriptional inflammatory responses. These results provide a solid foundation for future investigations to elucidate the underlying transcriptional regulatory mechanisms under the host inflammatory response. Also, the assumption that coexpressed genes that are functionally relevant are more likely to share some common transcriptional regulatory mechanism seems to be promising, making the proposed framework become essential in unravelling context-specific transcriptional regulatory interactions underlying diverse mammalian biological processes