Progress report on the ultra heavy cosmic ray experiment (AO178)

The Ultra Heavy Cosmic Ray Experiment (UHCRE) is based on a modular array of 192 side-viewing solid state nuclear track detector stacks. These stacks were mounted in sets of four in 48 pressure vessels employing sixteen peripheral Long Duration Exposure Facility (LDEF) trays. The extended duration of the LDEF mission has resulted in a greatly enhanced scientific yield from the UHCRE. The geometry factor for high energy cosmic ray nuclei, allowing for Earth shadowing, was 30 sq m-sr, giving a total exposure factor of 170 sq m-sr-y at an orbital inclination of 28.4 degrees. Scanning results indicate that about 3000 cosmic ray nuclei in the charge region with Z greater than 65 were collected. This sample is more than ten times the current world data in the field (taken to be the data set from the HEAO-3 mission plus that from the Ariel-6 mission) and is sufficient to provide the world's first statistically significant sample of actinide (Z greater than 88) cosmic rays. Results to date are presented including details of ultra-heavy cosmic ray nuclei, analysis of pre-flight and post-flight calibration events and details of track response in the context of detector temperature history. The integrated effect of all temperature and age related latent track variations cause a maximum charge shift of +/- 0.8 e for uranium and +/- 0.6 e for the platinum-lead group. The precision of charge assignment as a function of energy is derived and evidence for remarkably good charge resolution achieved in the UHCRE is considered. Astrophysical implications of the UHCRE charge spectrum are discussed

The LDEF ultra heavy cosmic ray experiment

The LDEF Ultra Heavy Cosmic Ray Experiment (UHCRE) used 16 side viewing LDEF trays giving a total geometry factor for high energy cosmic rays of 30 sq m sr. The total exposure factor was 170 sq m sr y. The experiment is based on a modular array of 192 solid state nuclear track detector stacks, mounted in sets of four in 48 pressure vessels. The extended duration of the LDEF mission has resulted in a greatly enhanced potential scientific yield from the UHCRE. Initial scanning results indicate that at least 1800 cosmic ray nuclei with Z greater than 65 were collected, including the world's first statistically significant sample of actinides. Post flight work to date and the current status of the experiment are reviewed

Transfer of in vivo primed transgenic T cells supports allergic lung inflammation and FIZZ1 and Ym1 production in an IL-4Rα and STAT6 dependent manner

<p>Abstract</p> <p>Background</p> <p>CD4+ T helper type 2 (T_H2) cells, their cytokines IL-4, IL-5 and IL-13 and the transcription factor STAT6 are known to regulate various features of asthma including lung inflammation, mucus production and airway hyperreactivity and also drive alternative activation of macrophages (AAM). However, the precise roles played by the IL-4/IL-13 receptors and STAT6 in inducing AAM protein expression and modulating specific features of airway inflammation are still unclear. Since T_H2 differentiation and activation plays a pivotal role in this disease, we explored the possibility of developing an asthma model in mice using T cells that were differentiated <it>in vivo</it>.</p> <p>Results</p> <p>In this study, we monitored the activation and proliferation status of adoptively transferred allergen-specific naïve or <it>in vivo </it>primed CD4+ T cells. We found that both the naïve and <it>in vivo </it>primed T cells expressed similar levels of CD44 and IL-4. However, <it>in vivo </it>primed T cells underwent reduced proliferation in a lymphopenic environment when compared to naïve T cells. We then used these <it>in vivo </it>generated effector T cells in an asthma model. Although there was reduced inflammation in mice lacking IL-4Rα or STAT6, significant amounts of eosinophils were still present in the BAL and lung tissue. Moreover, specific AAM proteins YM1 and FIZZ1 were expressed by epithelial cells, while macrophages expressed only YM1 in RAG2^-/-mice. We further show that FIZZ1 and YM1 protein expression in the lung was completely dependent on signaling through the IL-4Rα and STAT6. Consistent with the enhanced inflammation and AAM protein expression, there was a significant increase in collagen deposition and smooth muscle thickening in RAG2^-/-mice compared to mice deficient in IL-4Rα or STAT6.</p> <p>Conclusions</p> <p>These results establish that transfer of <it>in vivo </it>primed CD4+ T cells can induce allergic lung inflammation. Furthermore, while IL-4/IL-13 signaling through IL-4Rα and STAT6 is essential for AAM protein expression, lung inflammation and eosinophilia are only partially dependent on this pathway. Further studies are required to identify other proteins and signaling pathways involved in airway inflammation.</p

Reproducibility of coronary artery diameter assessments in magnetic resonance coronary angiography: phantom study

This report describes the development of a deformable model for the automatic delineation of coronary artery cross-sectional areas with magnetic resonance imaging. The method is validated with coronary artery phantoms of varying diameters and images with different levels of signal-to-noise ratios. The reproducibility of the technique was examined with simulated geometrical shifts and motions during data acquisition. The experimental results indicate a very high reproducibility and low inter-observers variability of the technique, suggesting its suitability for non-invasive assessment of serial changes of vessel dilatation following pharmacological intervention

A New Smartphone-Based Optic Nerve Head Biometric for Verification and Change Detection

Purpose: Lens adapted smartphones are being used regularly instead of ophthalmoscopes. The most common causes of preventable blindness in the world, which are glaucoma and diabetic retinopathy, can develop asymptomatic changes to the optic nerve head (ONH) especially in the developing world where there is a dire shortage of ophthalmologists but ubiquitous mobile phones. We developed a proof-of-concept ONH biometric (application [APP]) to use as a routine biometric on a mobile phone. The unique blood vessel pattern is verified if it maps on to a previously enrolled image. Methods: The iKey APP platform comprises three deep neural networks (DNNs) developed from anonymous ONH images: the graticule blood vessel (GBV) and the blood vessel specific feature (BVSF) DNNs were trained on unique blood vessel vectors. A non-feature specific (NFS) baseline ResNet50 DNN was trained for comparison. Results: Verification reached an accuracy of 97.06% with BVSF, 87.24% with GBV and 79.8% using NFS. Conclusions: A new ONH biometric was developed with a hybrid platform of ONH algorithms for use as a verification biometric on a smartphone. Failure to verify will alert the user to possible changes to the image, so that silent changes may be observed before sight threatening disease progresses. The APP retains a history of all ONH images. Future longitudinal analysis will explore the impact of ONH changes to the iKey biometric platform. Translational Relevance: Phones with iKey will host ONH images for biometric protection of both health and financial data. The ONH may be used for automatic screening by new disease detection DNNs

Expression of neuroimmune semaphorins 4A and 4D and their receptors in the lung is enhanced by allergen and vascular endothelial growth factor

<p>Abstract</p> <p>Background</p> <p>Semaphorins were originally identified as molecules regulating <b>a </b>functional activity of axons in the nervous system. Sema4A and Sema4D were the first semaphorins found to be expressed on immune cells and were termed "immune semaphorins". It is known that Sema4A and Sema4D bind Tim-2 and CD72 expressed on leukocytes and PlexinD1 and B1 present on non-immune cells. These neuroimmune semaphorins and their receptors have been shown to play critical roles in many physiological and pathological processes including neuronal development, immune response regulation, cancer, autoimmune, cardiovascular, renal, and infectious diseases. However, the expression and regulation of Sema4A, Sema4D, and their receptors in normal and allergic lungs is undefined.</p> <p>Results</p> <p>Allergen treatment and lung-specific vascular endothelial growth factor (VEGF) expression induced asthma-like pathologies in the murine lungs. These experimental models of allergic airway inflammation were used for the expression analysis of immune semaphorins and their receptors employing immunohistochemistry and flow cytometry techniques. We found that besides accessory-like cells, Sema4A was also detected on bronchial epithelial and smooth muscle cells, whereas Sema4D expression was high on immune cells such as T and B lymphocytes. Surprisingly, under inflammation various cell types including macrophages, lymphocytes, and granulocytes in the lung expressed Tim-2, a previously defined marker for Th2 cells. CD72 was found on lung immune, inflammatory, and epithelial cells. Bronchial epithelial cells were positive for both plexins, whereas some endothelial cells selectively expressed Plexin D1. Plexin B1 expression was also detected on lung DC. Both allergen and VEGF upregulated the expression of neuroimmune semaphorins and their receptors in the lung tissue. However, the lung tissue Sema4A-Tim2 expression was rather weak, whereas Sema4D-CD72 ligand-receptor pair was vastly upregulated by allergen. Soluble Sema4D protein was present in the lung lysates and a whole Sema4A protein plus its dimer were readily detected in the bronchoalveolar (BAL) fluids under inflammation.</p> <p>Conclusions</p> <p>This study clearly shows that neuroimmune semaphorins Sema4A and Sema4D and their receptors might serve as potential markers for the allergic airway inflammatory diseases. Our current findings pave the way for further investigations of the role of immune semaphorins in inflammation and their use as potential therapeutic targets for the inflammatory lung conditions.</p

IL-4 engagement of the type 1 IL-4 receptor complex enhances mouse eosinophil migration to eotaxin-1 in vitro

Background Previous work from our laboratory demonstrated that IL-4Rα expression on a myeloid cell type was responsible for enhancement of Th2-driven eosinophilic inflammation in a mouse model of allergic lung inflammation. Subsequently, we have shown that IL-4 signaling through type I IL-4 receptors on monocytes/macrophages strongly induced activation of the IRS-2 pathway and a subset of genes characteristic of alternatively activated macrophages. The direct effect(s) of IL-4 and IL-13 on mouse eosinophils are not clear. The goal of this study was determine the effect of IL-4 and IL-13 on mouse eosinophil function. Methods Standard Transwell chemotaxis assay was used to assay migration of mouse eosinophils and signal transduction was assessed by Western blotting. Results Here we determined that (i) mouse eosinophils express both type I and type II IL-4 receptors, (ii) in contrast to human eosinophils, mouse eosinophils do not chemotax to IL-4 or IL-13 although (iii) pre-treatment with IL-4 but not IL-13 enhanced migration to eotaxin-1. This IL-4-mediated enhancement was dependent on type I IL-4 receptor expression: γC-deficient eosinophils did not show enhancement of migratory capacity when pre-treated with IL-4. In addition, mouse eosinophils responded to IL-4 with the robust tyrosine phosphorylation of STAT6 and IRS-2, while IL-13-induced responses were considerably weaker. Conclusions The presence of IL-4 in combination with eotaxin-1 in the allergic inflammatory milieu could potentiate infiltration of eosinophils into the lungs. Therapies that block IL-4 and chemokine receptors on eosinophils might be more effective clinically in reducing eosinophilic lung inflammation

Comparision of antibiotics on growth performance of weanling pigs in a commerical environment

A total of 320 weanling pigs (10.7 lb and 14 ± 3 d of age, PIC) was used to determine the effects of antibiotics and an antibiotic alternative on nursery pig performance. Pigs were fed one of 5 experimental diets: 1) control with no antimicrobials; 2) carbadox (50 g/ton); 3) Denagard/CTC (35 g/ton Denagard™, 400 g/ton Chlortetracycline); 4) Neo-Terramycin® (140 g/ton Neomycin Sulfate, 140 g/ton Oxytetracycline HCl); 5) Bio Mos (0.3%, mannanoligosaccharide). Overall (d 0 to 31 post-weaning), pigs fed the diet containing Denagard/CTC had the greatest (P\u3c0.05) ADG and ADFI compared to pigs fed all other treatment diets. Pigs fed the diet containing Neo-Terramycin had greater (P\u3c0.05) ADG compared to pigs fed the control diet or diets containing Carbadox or Bio Mos. In addition, pigs fed the diet containing Neo-Terramycin had greater (P\u3c0.05) ADFI compared to pigs fed the control diet or the diet containing Bio Mos. In conclusion, the addition of carbadox and Bio Mos did not result in improved growth performance compared to pigs fed the control diet. However, improvements were seen in average daily gain and daily feed intake with the addition of Denagard/CTC and Neo-Terramycin. Commercial operations need to determine which feed additives improve nursery pig performance in their individual production systems.; Swine Day, 2003, Kansas State University, Manhattan, KS, 200