Hepatitis C virus point-of-care RNA testing: Experience from screening an entire high-security Australian prison population over 3 days.

OBJECTIVE: Point-of-care testing for hepatitis C virus (HCV) in high-risk populations is key to diagnosing and eliminating HCV. We aimed to test all occupants for HCV in an entire prison. METHODS: All consenting participants at the Brisbane Women's Correctional Centre were tested for HCV over 3 days using fingerstick samples. Participants with HCV were linked to care by a Nurse Practitioner experienced in HCV management. RESULTS: 211 of 244 participants of the prison population at the time (86%) consented and were tested. 17 participants (8%) had HCV, of who 14 commenced antiviral therapy ≤1 week of testing, 1 was later approved for antiviral therapy in consultation with a physician, and 2 due for release were followed-up and linked to care in the community. Education and counselling provided before testing was rated as very good or excellent by 47% of participants. CONCLUSIONS: Testing occupants in a high-security prison of this size is feasible and can provide an overview of HCV infectivity. Testing combined with linkage to care will support the elimination of HCV in this high-risk population. IMPLICATIONS FOR PUBLIC HEALTH: Point-of-care testing for HCV in prisons with dedicated clinicians, resources, and partnerships, particularly at prison entry, can contribute to eliminating HCV in Australia by 2030.

Emulating Near-Roadway Exposure to Traffic-Related Air Pollution via Real-Time Emissions from a Major Freeway Tunnel System.

Epidemiological and toxicological studies continue to demonstrate correlative and causal relationships between exposure to traffic-related air pollution and various metrics of adverse pulmonary, cardiovascular, and neurological health effects. The key challenge for in vivo studies is replicating real-world, near-roadway exposure dynamics in laboratory animal models that mimic true human exposures. The advantage of animal models is the accelerated time scales to show statistically significant physiological and/or behavioral response. This work describes a novel exposure facility adjacent to a major freeway tunnel system that provides a platform for real-time chronic exposure studies. The primary conclusion is that particulate matter (PM) concentrations at this facility are routinely well below the National Ambient Air Quality Standards (NAAQS), but studies completed to date still demonstrate significant neurological and cardiovascular effects. Internal combustion engines produce large numbers of ultrafine particles that contribute negligible mass to the atmosphere relative to NAAQS regulated PM2.5 but have high surface area and mobility in the body. It is posited here that current federal and state air quality standards are thus insufficient to fully protect human health, most notably the developing and aging brain, due to regulatory gaps for ultrafine particles.

Novel multi-functional europium-doped gadolinium oxide nanoparticle aerosols facilitate the study of deposition in the developing rat lung.

Ambient ultrafine particulate matter (UPM), less than 100 nm in size, has been linked to the development and exacerbation of pulmonary diseases. Age differences in susceptibility to UPM may be due to a difference in delivered dose as well as age-dependent differences in lung biology and clearance. In this study, we developed and characterized aerosol exposures to novel metal oxide nanoparticles containing lanthanides to study particle deposition in the developing postnatal rat lung. Neonatal, juvenile and adult rats (1, 3 and 12 weeks old) were nose only exposed to 380 µg m(-3) of ∼30 nm europium doped gadolinium oxide nanoparticles (Gd2O3:Eu(3+)) for 1 h. The deposited dose in the nose, extrapulmonary airways and lungs was determined using inductively-coupled plasma mass spectroscopy. The dose of deposited particles was significantly greater in the juvenile rats at 2.22 ng per g body weight compared to 1.47 ng per g and 0.097 ng per g for the adult and neonate rats, respectively. Toxicity was investigated in bronchoalveolar lavage fluid (BALF) by quantifying recovered cell types, and measuring lactate dehydrogenase activity and total protein. The toxicity data suggests that the lanthanide particles were not acutely toxic or inflammatory with no increase in neutrophils or lactate dehydrogenase activity at any age. Juvenile and adult rats had the same mass of deposited NPs per gram of lung tissue, while neonatal rats had significantly less NPs deposited per gram of lung tissue. The current study demonstrates the utility of novel lanthanide-based nanoparticles to study inhaled particle deposition in vivo and has important implications for nanoparticles delivery to the developing lung either as therapies or as a portion of particulate matter air pollution.

Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles.

This study examined airway structure changes in adult rats after a long recovery period due to sub-chronic juvenile exposure to ozone and ultrafine particles that have a high organic fraction. Neonatal male Sprague-Dawley rats were exposed during lung development to 3 cycles of 0.5 ppm ozone from postnatal day 7 through 25. Two different exposure patterns were used: 5-day exposure per week (Ozone52) or 2-day exposure per week (Ozone25) with or without co-exposure to ultrafine particles (OPFP5252, OPFP5225). Airway architecture was evaluated at 81 days of age, after 56 days of continued development beyond the exposure period in filtered air (FA). By analyzing CT images from lung airway casts, we determined airway diameter, length, branching angle, and rotation angle for most conducting airways. Compared with the FA control group, the Ozone52 group showed significant decreases in airway diameter in generations larger than 10 especially in the right diaphragmatic lobe and in airway length in distal generations, while changes in airway structure due to the Ozone25 exposure were not appreciable. Interaction effects of ozone and ultrafine particle exposures were not significant. These results suggest that airway alterations due to postnatal ozone exposure are not limited to the distal region but occur extensively from the middle to distal conducting airways. Further, alterations due to early ozone exposure do not recover nearly 2 months after exposure has ceased demonstrating a persistent airway structural change following an early life exposure to ozone.

Small particles disrupt postnatal airway development.

Increasing numbers of epidemiologic studies associate air pollution exposure in children with decreased lung function development. The objective of this study was to examine the effects of exposure to combustion-generated fine [230 and 212 nm number mean aerodynamic particle diameter (NMAD)] to ultrafine (73 nm NMAD) particles differing in elemental (EC) and organic (OC) carbon content on postnatal airway development in rats. Neonatal Sprague-Dawley rats were exposed from postnatal day 7 through 25, and lung function and airway architecture were evaluated 81 days of age. In a separate group of rats, cell proliferation was examined after a single particle exposure at 7 days of age. Early life exposure to 73 nm high OC/EC particles altered distal airway architecture and resulted in subtle changes in lung mechanics. Early life exposure to 212 nm high OC/EC particles did not alter lung architecture but did alter lung mechanics in a manner suggestive of central airway changes. In contrast, early life exposure to 230 nm low OC/EC particles did not alter lung architecture or mechanics. A single 6-h exposure to 73 nm high OC/EC particle decreased airway cell proliferation, whereas 212 nm high OC/EC particles increased it and 230 nm low OC/EC particles did not. The early life exposure to ultrafine, high OC/EC particles results in persistent alterations in distal airway architecture that is characterized by an initial decrease in airway cell proliferation.

Partnership working with independent providers.

The Department of Health in England want to see NHS commissioners and providers capitalize upon the expertise of the independent sector for the benefit of NHS patients. In preparing for the future what does the sector have to offer NHS nurses and how will this benefit patient care? This paper examines the role of independent providers and the way they are helping NHS commissioners and providers to break new ground in delivering more accessible and convenient care for NHS patients at home.

An automated self-similarity analysis of the pulmonary tree of the Sprague-Dawley rat.

We present the results of an automated analysis of the morphometry of the pulmonary airway trees of the Sprague-Dawley rat. Our work is motivated by a need to inform lower-dimensional mathematical models to prescribe realistic boundary conditions for multiscale hybrid models of rat lung mechanics. Silicone casts were made from three age-matched, male Sprague-Dawley rats, immersed in a gel containing a contrast agent and subsequently imaged with magnetic resonance (MR). From a segmentation of this data, we extracted a connected graph, representing the airway centerline. Segment statistics (lengths and diameters) were derived from this graph. To validate this MR imaging/digital analysis method, airway segment measurements were compared with nearly 1,000 measurements collected by hand using an optical microscope from one of the rat lung casts. To evaluate the reproducibility of the MR imaging/digital analysis method, two lung casts were each imaged three times with randomized orientations in the MR bore. Diameters and lengths of randomly selected airways were compared among each of the repeated imaging datasets to estimate the variability. Finally, we analyzed the morphometry of the airway tree by assembling individual airway segments into structures that span multiple generations, which we call branches. We show that branches not segments are the fundamental repeating unit in the rat lung and develop simple mathematical relationships describing these structures for the entire lung. Our analysis shows that airway diameters and lengths have both a deterministic and stochastic character.

Effects of fertilization and fungal and insect attack on systemic protein defenses of austrian pine.

Despite their economic and ecological importance, defense responses of conifers to pests are little understood. In a 3-year experiment, we monitored systemic fungal (Diplodia pinea)- and insect (Neodiprion sertifer)-induced defense protein activities and total soluble proteins in needles and phloem of Austrian pine (Pinus nigra) across a soil fertility gradient. In both years, total soluble protein content of foliage and phloem declined with increasing fertility across induction treatments, while defensive protein activities generally increased with increasing fertility. In 2005, total soluble protein content in branch phloem was increased by fungal inoculation of the stem. Peroxidase activity was suppressed in needles by insect defoliation in 2006, while polyphenol oxidase activity was systemically induced in branch phloem by insect attack in 2005. Trypsin inhibitor activities in phloem did not respond to any induction or fertility treatment. Nutritive quality of Austrian pine tissue declined with increasing fertility, while several protein-based defenses simultaneously increased.

Cross-induction of systemic induced resistance between an insect and a fungal pathogen in Austrian pine over a fertility gradient.

Evidence for cross-induction of systemic resistance or susceptibility in plant-fungus-herbivore interactions is mostly derived from herbaceous model systems and not perennial woody plants. Furthermore, the effects of environmental variables such as soil fertility on these tripartite interactions are generally unknown. This study examined cross-induction of systemic resistance in Pinus nigra (Austrian pine) to infection by Sphaeropsis sapinea (a fungal pathogen), or feeding by Neodiprion sertifer (European pine sawfly), by prior induction with either S. sapinea or N. sertifer, over a fertility gradient. In a replicated 3-year study, cross-induction of systemic induced resistance (SIR) was found to be both asymmetric within a single year and variable between years. Prior induction with insect defoliation induced SIR to subsequent fungal challenge in 2006 but not in 2005. In 2005, a fertility-independent negative systemic effect of the fungal infection on herbivore growth was detected while herbivore survival was affected by a significant interaction between induction treatment and fertility level in 2006. Prior infection by the fungus induced SIR against the same fungus in both years regardless of fertility levels. This is the first report of whole-plant SIR against a defoliating insect induced by a fungal pathogen and vice versa, under variable nutrient availability, in a conifer or any other tree.