The effects of addition of a series of organoamine molecules on the luminescence of porous silicon has been examined by steady-state photoluminescence (PL) and Fourier transform infrared spectroscopies. These samples, prepared nonanodically via stain etching techniques and characterized by atomic force microscopy, show dramatic quenching of visible PL upon addition of dilute solutions of the above Lewis base adsorbates. The fractional changes in integrated PL intensity as a function of quencher concentration obey a simple equilibrium model, demonstrating Langmuir-type behavior from which equilibrium constants can be calculated. An observation concomitant with this loss of PL is a diminution of the silicon hydride stretching frequencies near 2100 cm−1.

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Lung mastocytosis and antigen-induced bronchoconstriction are common features in allergic asthmatics. It is therefore important that animal models of asthma show similar features of mast cell inflammation and reactivity to inhaled allergen. We hypothesized that house dust mite (HDM) would induce mastocytosis in the lung and that inhalation of HDM would trigger bronchoconstriction. Mice were sensitized with intranasal HDM extract, and the acute response to nebulized HDM or the mast cell degranulating compound 48/80 was measured with respiratory input impedance. Using the constant-phase model we calculated Newtonian resistance (Rn) reflecting the conducting airways, tissue dampening (G), and lung elastance (H). Bronchoalveolar lavage fluid was analyzed for mouse mast cell protease-1 (mMCP-1). Lung tissue was analyzed for cytokines, histamine, and α-smooth muscle actin (α-SMA), and histological slides were stained for mast cells. HDM significantly increased Rn but H and G remained unchanged. HDM significantly expanded mast cells compared with control mice; at the same time mMCP-1, α-SMA, Th2 cytokines, and histamine were significantly increased. Compound 48/80 inhalation caused bronchoconstriction and mMCP-1 elevation similarly to HDM inhalation. Bronchoconstriction was eliminated in mast cell-deficient mice. We found that antigen-induced acute bronchoconstriction has a distinct phenotype in mice. HDM sensitization caused lung mastocytosis, and we conclude that inhalation of HDM caused degranulation of mast cells leading to an acute bronchoconstriction without affecting the lung periphery and that mast cell-derived mediators are responsible for the development of the HDM-induced bronchoconstriction in this model.

After the first detection of myrtle rust (Austropuccinia psidii) on mainland New Zealand in May 2017, the Ministry for Primary Industries sought information about how weather conditions would affect regional and seasonal risk of disease establishment to help plan the incursion response. Using internationally published information, a pathogen-process model was developed to predict infection, latent period and sporulation in relation to weather variables (temperature, relative humidity and solar radiation). This Myrtle Rust Process Model (MRPM) was implemented by the National Institute of Water and Atmospheric Research Limited using numerical weather model data to produce weekly maps of potential risk. Predicted risk was greatest in northern North Island and decreased further south, but was still substantial in coastal areas of the north-western South Island during summer and autumn. Risk was low in southern coastal areas of the South Island and the lowest risk occurred in mountainous areas, particularly in the South Island. Retrospective analysis of surveillance data showed that the MRPM accurately predicted geographic risk and it is currently in use for tactical planning of incursion surveillance and organism management.

Background While many of the contributing cell types and mediators of allergic asthma are known, less well understood are the factors that induce allergy in the first place. Amongst the mediators speculated to affect initial allergen sensitization and the development of pathogenic allergic responses to innocuous inhaled antigens and allergens are exogenously- or endogenously-generated reactive oxygen species (ROS) and reactive nitrogen species (RNS). Scope of Review The interactions between ROS/RNS, dendritic cells (DCs), and CD4+ T cells, as well as their modulation by lung epithelium, are of critical importance for the genesis of allergies that later manifest in allergic asthma. Therefore, this review will primarily focus on the initiation of pulmonary allergies and the role that ROS/RNS may play in the steps therein, using examples from our own work on the roles of NO2 exposure and airway epithelial NF-κB activation. Major Conclusions Endogenously-generated ROS/RNS and those encountered from environmental sources interact with epithelium, DCs, and CD4+ T cells to orchestrate allergic sensitization through modulation of the activities of each of these cell types, which quatitiatively and qualitatively dictate the degree and type of the allergic asthma phenotype. General Significance Knowledge of the effects of ROS/RNS at the molecular and cellular levels has the potential to provide powerful insight into the balance between inhalational tolerance (the typical immunologic response to an innocuous inhaled antigen) and allergy, as well as to potentially provide mechanistic targets for the prevention and treatment of asthma.