A Wide-Field CCD Survey for Centaurs and Kuiper Belt Objects

A modified Baker-Nunn camera was used to conduct a wide-field survey of 1428 square degrees of sky near the ecliptic in search of bright Kuiper Belt objects and Centaurs. This area is an order of magnitude larger than any previously published CCD survey for Centaurs and Kuiper Belt Objects. No new objects brighter than red magnitude m=18.8 and moving at a rate 1"/hr to 20"/hr were discovered, although one previously discovered Centaur 1997 CU26 Chariklo was serendipitously detected. The parameters of the survey were characterized using both visual and automated techniques. From this survey the empirical projected surface density of Centaurs was found to be SigmaCentaur(m<18.8)=7.8(+16.0 -6.6)x10^-4 per square degree and we found a projected surface density 3sigma upper confidence limit for Kuiper Belt objects of SigmaKBO(m< 18.8)<4.1x10^-3 per square degree. We discuss the current state of the cumulative luminosity functions of both Centaurs and Kuiper Belt objects. Through a Monte Carlo simulation we show that the size distribution of Centaurs is consistent with a q=4 differential power law, similar to the size distribution of the parent Kuiper Belt Objects. The Centaur population is of order 10^7 (radius > 1 km) assuming a geometric albedo of 0.04. About 100 Centaurs are larger than 50 km in radius, of which only 4 are presently known. The current total mass of the Centaurs is 10^-4 Earth Masses. No dust clouds were detected resulting from Kuiper Belt object collisions, placing a 3sigma upper limit <600 collisionally produced clouds of m<18.8 per year.Comment: 13 pages, 5 figures, Accepted for Publication in A

Study on Occupational Allergy Risks (SOLAR II) in Germany: Design and methods

<p>Abstract</p> <p>Background</p> <p>SOLAR II is the 2^ndfollow-up of a population-based cohort study that follows the participants of ISAAC Phase Two recruited in Munich and Dresden in 1995/6. A first follow-up study was conducted 2002 and 2003 (SOLAR I). The aims of SOLAR II were to investigate the course of atopic diseases over puberty taking environmental and occupational risk factors into account. This paper describes the methods of the 2^ndfollow-up carried out from 2007 to 2009 and the challenges we faced while studying a population-based cohort of young adults.</p> <p>Methods</p> <p>Wherever possible, the same questionnaire instruments were used throughout the studies. They included questions on respiratory and allergic diseases, domestic and occupational exposure and work related stress. Furthermore, clinical examinations including skin prick tests, spirometry and bronchial challenge with methacholine, exhaled nitric oxide (FeNO) and blood samples were employed at baseline and 2^ndfollow-up. As information from three studies was available, multiple imputation could be used to handle missing data.</p> <p>Results</p> <p>Of the 3053 SOLAR I study participants who had agreed to be contacted again, about 50% had moved in the meantime and had to be traced using phone directories and the German population registries. Overall, 2904 of these participants could be contacted on average five years after the first follow-up. From this group, 2051 subjects (71%) completed the questionnaire they received via mail. Of these, 57% participated at least in some parts of the clinical examinations. Challenges faced included the high mobility of this age group. Time constraints and limited interest in the study were substantial. Analysing the results, selection bias had to be considered as questionnaire responders (54%) and those participating in the clinical part of the study (63%) were more likely to have a high parental level of education compared to non-participants (42%). Similarly, a higher prevalence of parental atopy (e.g. allergic rhinitis) at baseline was found for participants in the questionnaire part (22%) and those participating in the clinical part of the study (27%) compared to non-participants (11%).</p> <p>Conclusions</p> <p>In conclusion, a 12-year follow-up from childhood to adulthood is feasible resulting in a response of 32% of the baseline population. However, our experience shows that researchers need to allocate more time to the field work when studying young adults compared to other populations.</p

The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma

Atopic dermatitis (AD) is an inflammatory disease characterized by pruritic skin lesions. The pathogenesis of AD may include disrupted epidermal barrier function, immunodysregulation, and IgE-mediated sensitization to food and environmental allergens. AD is also part of a process called the atopic march, a progression from AD to allergic rhinitis and asthma. This has been supported by multiple cross-sectional and longitudinal studies and experimental data. Research on the mechanisms of AD has been centered on the adaptive immune system with an emphasis on the T-helper 1 (Th1)-Th2 paradigm. Recently, the conceptual focus has largely shifted to include a primary defect in the epithelial barrier as an initial event in AD providing a significant insight into the disease initiation and pointing to a complex secondary interplay of environmental and immunological sequelae with barrier disruption. Further understanding of AD will help the development of more effective treatment for AD and ultimately, preventative algorithms for the atopic march. In this review we highlight recent advances in our understanding of the pathogenesis of AD and the atopic march

Fetal and infant origins of asthma

Previous studies have suggested that asthma, like other common diseases, has at least part of its origin early in life. Low birth weight has been shown to be associated with increased risks of asthma, chronic obstructive airway disease, and impaired lung function in adults, and increased risks of respiratory symptoms in early childhood. The developmental plasticity hypothesis suggests that the associations between low birth weight and diseases in later life are explained by adaptation mechanisms in fetal life and infancy in response to various adverse exposures. Various pathways leading from adverse fetal and infant exposures to growth adaptations and respiratory health outcomes have been studied, including fetal and early infant growth patterns, maternal smoking and diet, children’s diet, respiratory tract infections and acetaminophen use, and genetic susceptibility. Still, the specific adverse exposures in fetal and early postnatal life leading to respiratory disease in adult life are not yet fully understood. Current studies suggest that both environmental and genetic factors in various periods of life, and their epigenetic mechanisms may underlie the complex associations of low birth weight with respiratory disease in later life. New well-designed epidemiological studies are needed to identify the specific underlying mechanisms. This review is focused on specific adverse fetal and infant growth patterns and exposures, genetic susceptibility, possible respiratory adaptations and perspectives for new studies

Reconstructing Metaphorical Meaning

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