Redistribution Of Air Within The Lungs May Potentiate "Fright" Bradycardia In Submerged Crocodiles (Crocodylus porosus)

1. Voluntary undisturbed dives by Crocodylus porosus were short in duration (3.08 + 1.87 min, mean + SD) and accompanied by a small but significant bradycardia (14.3 + 5.9% drop). 2. When crocodiles were disturbed underwater there was a rapid onset of "fright" bradycardia, to 65 + 6.0% of surface heart rates and dive durations were prolonged to 19.6 + 1.8 min. 3. The development of "fright" bradycardia was not accompanied by any increase in intratracheal pressure or expulsion of lung gas. However, sustained contraction of the abdomen and expansion of the thorax revealed a redistribution of air anteriorly within the lungs. 4. We propose that the redistribution of air within the lungs may generate an afferent signal which potentiates the initiation of a severe, dive-prolonging bradycardia

Near Fatal and Fatal Asthma and Air Pollution – are we missing an opportunity to ask key questions?

There is an increasing body of evidence supporting the link between asthma attacks and air pollution in children. To our knowledge, there has only been one reported case of a fatal asthma attack in a child associated with air pollution and this was in the UK. This article considers why there is a lack of evidence on fatal/near-fatal asthma and air pollution. We also explore three challenges. First, fatal and near-fatal asthma events are rare and not yet well understood. Second, measuring and interpreting personal exposure to air pollution with sufficient temporal and spatial detail are challenging to interpret in the context of individual fatal or near-fatal asthma attacks. Third, current studies are not designed to answer the question of whether or to what extent air pollution is associated with fatal/near-fatal asthma attacks in children. Conclusive evidence is not yet available and systems of data collection for both air pollution and fatal and near-fatal asthma attacks should be enhanced to ensure risk can be determined and impact minimised

How do you explain the risk of air pollution to your patients?

.@ERStalk Environ & Health committee workshop concludes: HCPs vital to raising awareness of air pollution to patients http://ow.ly/pfOe301FoIg

Acute exposure of mice to high-dose ultrafine carbon black decreases susceptibility to pneumococcal pneumonia

<p>Abstract</p> <p>Background</p> <p>Epidemiological studies suggest that inhalation of carbonaceous particulate matter from biomass combustion increases susceptibility to bacterial pneumonia. <it>In vitro </it>studies report that phagocytosis of carbon black by alveolar macrophages (AM) impairs killing of <it>Streptococcus pneumoniae</it>. We have previously reported high levels of black carbon in AM from biomass smoke-exposed children and adults. We therefore aimed to use a mouse model to test the hypothesis that high levels of carbon loading of AM <it>in vivo </it>increases susceptibility to pneumococcal pneumonia.</p> <p>Methods</p> <p>Female outbred mice were treated with either intranasal phosphate buffered saline (PBS) or ultrafine carbon black (UF-CB in PBS; 500 μg on day 1 and day 4), and then infected with <it>S. pneumoniae </it>strain D39 on day 5. Survival was assessed over 72 h. The effect of UF-CB on AM carbon loading, airway inflammation, and a urinary marker of pulmonary oxidative stress was assessed in uninfected animals.</p> <p>Results</p> <p>Instillation of UF-CB in mice resulted a pattern of AM carbon loading similar to that of biomass-smoke exposed humans. In uninfected animals, UF-CB treated animals had increased urinary 8-oxodG (P = 0.055), and an increased airway neutrophil differential count (P < 0.01). All PBS-treated mice died within 72 h after infection with S<it>. pneumoniae</it>, whereas morbidity and mortality after infection was reduced in UF-CB treated animals (median survival 48 h vs. 30 h, P < 0.001). At 24 hr post-infection, UF-CB treated mice had lower lung and the blood S<it>. pneumoniae </it>colony forming unit counts, and lower airway levels of keratinocyte-derived chemokine/growth-related oncogene (KC/GRO), and interferon gamma.</p> <p>Conclusion</p> <p>Acute high level loading of AM with ultrafine carbon black particles <it>per se </it>does not increase the susceptibility of mice to pneumococcal infection <it>in vivo</it>.</p

Small-particle Inhaled Corticosteroid as First-line or Step-up Controller Therapy in Childhood Asthma

Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.Peer reviewedPublisher PD

Underground railway particulate matter and susceptibility to pneumococcal infection

Background Concentrations of particulate matter less than 10 microns (PM10) on underground railways are higher than those near urban roads. Traffic-related PM10 increases pneumococcal infection via increasing the expression of platelet-activating factor receptor (PAFR), a receptor co-opted by pneumococci to adhere to cells. To date, it is unknown whether underground railway PM10 increases pneumococcal infection. This study sought to determine the effect of London Underground (LU) PM10 on; i) pneumococcal adhesion to airway cells, and ii) susceptibility to pneumococcal disease. Methods A549 cells and human primary airway epithelial cells were cultured with 20 µg/mL PM10 from the Bakerloo (B-PM10) and Jubilee (J-PM10) line platforms of Baker Street station. PAFR expression was assessed by flow cytometry, and pneumococcal adhesion by colony forming unit (CFU) counts. Traffic-related PM10 was collected next to a main road near the station's entrance. The PAFR blocker CV3988 and the antioxidant N-acetyl cysteine were used to assess the role of PAFR-mediated pneumococcal adhesion and oxidative stress respectively. Pneumococcal infection of mice was done after exposure to 3×80 μg doses of intranasal LU-PM10. Findings In A549 cells, human primary nasal cells, and human primary bronchial epithelial cells, B-PM10 and J-PM10 increased PAFR expression and pneumococcal adhesion. Stimulated adhesion was abrogated by CV3988 and N-acetyl cysteine. Traffic-related PM10 stimulated increased adhesion compared with B-PM10. B-PM10 and J-PM10 increased lung and blood CFU and mortality in mice. Treatment of B-PM10-exposed mice with CV3988 reduced blood CFU. Interpretation LU-PM10 increases pneumococcal adhesion to airway cells and susceptibility to invasive disease in mice

Association between Landscape Factors and Spatial Patterns of Plasmodium knowlesi Infections in Sabah, Malaysia.

The zoonotic malaria species Plasmodium knowlesi has become the main cause of human malaria in Malaysian Borneo. Deforestation and associated environmental and population changes have been hypothesized as main drivers of this apparent emergence. We gathered village-level data for P. knowlesi incidence for the districts of Kudat and Kota Marudu in Sabah state, Malaysia, for 2008-2012. We adjusted malaria records from routine reporting systems to reflect the diagnostic uncertainty of microscopy for P. knowlesi. We also developed negative binomial spatial autoregressive models to assess potential associations between P. knowlesi incidence and environmental variables derived from satellite-based remote-sensing data. Marked spatial heterogeneity in P. knowlesi incidence was observed, and village-level numbers of P. knowlesi cases were positively associated with forest cover and historical forest loss in surrounding areas. These results suggest the likelihood that deforestation and associated environmental changes are key drivers in P. knowlesi transmission in these areas