The atmospheric effects of stratospheric aircraft: A topical review

In the late 1960s the aircraft industry became interested in developing a fleet of supersonic transports (SSTs). Between 1972 and 1975, the Climatic Impact Assessment Program (CIAP) studied the possible environmental impact of SSTs. For environmental and economic reasons, the fleet of SSTs was not developed. The Upper Atmosphere Research Program (UARP) has recently undertaken the responsibility of directing scientific research needed to assess the atmospheric impact of supersonic transports. The UARP and the High-Speed Research Program asked Harold Johnston to review the current understanding of aircraft emissions and their effect on the stratosphere. Johnston and his colleagues have recently re-examined the SST problem using current models for stratospheric ozone chemistry. A unique view is given here of the current scientific issues and the lessons learned since the beginning of CIAP, and it links the current research program with the assessment process that began two years ago

Results of EVA/mobile transporter space station truss assembly tests

Underwater neutral buoyance tests were conducted to evaluate the use of a Mobile Transporter concept in conjunction with EVA astronauts to construct the Space Station Freedom truss structure. A three-bay orthogonal tetrahedral truss configuration with a 15 foot square cross section was repeatedly assembled by a single pair of pressure suited test subjects working from the Mobile Transporter astronaut positioning devices (mobile foot restraints). The average unit assembly time (which included integrated installation of utility trays) was 27.6 s/strut, or 6 min/bay. The results of these tests indicate that EVA assembly of space station size structures can be significantly enhanced when using a Mobile Transporter equipped with astronaut positioning devices. Rapid assembly time can be expected and are dependent primarily on the rate of translation permissible for on-orbit operations. The concept used to demonstate integrated installation of utility trays requires minimal EVA handling and consequentially, as the results show, has little impact on overall assembly time

Transcriptional profile of isoproterenol-induced cardiomyopathy and comparison to exercise-induced cardiac hypertrophy and human cardiac failure

<p>Abstract</p> <p>Background</p> <p>Isoproterenol-induced cardiac hypertrophy in mice has been used in a number of studies to model human cardiac disease. In this study, we compared the transcriptional response of the heart in this model to other animal models of heart failure, as well as to the transcriptional response of human hearts suffering heart failure.</p> <p>Results</p> <p>We performed microarray analyses on RNA from mice with isoproterenol-induced cardiac hypertrophy and mice with exercise-induced physiological hypertrophy and identified 865 and 2,534 genes that were significantly altered in pathological and physiological cardiac hypertrophy models, respectively. We compared our results to 18 different microarray data sets (318 individual arrays) representing various other animal models and four human cardiac diseases and identified a canonical set of 64 genes that are generally altered in failing hearts. We also produced a pairwise similarity matrix to illustrate relatedness of animal models with human heart disease and identified ischemia as the human condition that most resembles isoproterenol treatment.</p> <p>Conclusion</p> <p>The overall patterns of gene expression are consistent with observed structural and molecular differences between normal and maladaptive cardiac hypertrophy and support a role for the immune system (or immune cell infiltration) in the pathology of stress-induced hypertrophy. Cross-study comparisons such as the results presented here provide targets for further research of cardiac disease that might generally apply to maladaptive cardiac stresses and are also a means of identifying which animal models best recapitulate human disease at the transcriptional level.</p

Impaired perception of facial motion in autism spectrum disorder

Copyright: © 2014 O’Brien et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.This article has been made available through the Brunel Open Access Publishing Fund.Facial motion is a special type of biological motion that transmits cues for socio-emotional communication and enables the discrimination of properties such as gender and identity. We used animated average faces to examine the ability of adults with autism spectrum disorders (ASD) to perceive facial motion. Participants completed increasingly difficult tasks involving the discrimination of (1) sequences of facial motion, (2) the identity of individuals based on their facial motion and (3) the gender of individuals. Stimuli were presented in both upright and upside-down orientations to test for the difference in inversion effects often found when comparing ASD with controls in face perception. The ASD group’s performance was impaired relative to the control group in all three tasks and unlike the control group, the individuals with ASD failed to show an inversion effect. These results point to a deficit in facial biological motion processing in people with autism, which we suggest is linked to deficits in lower level motion processing we have previously reported

Meta-analysis of genome-wide association studies of asthma in ethnically diverse North American populations.

Asthma is a common disease with a complex risk architecture including both genetic and environmental factors. We performed a meta-analysis of North American genome-wide association studies of asthma in 5,416 individuals with asthma (cases) including individuals of European American, African American or African Caribbean, and Latino ancestry, with replication in an additional 12,649 individuals from the same ethnic groups. We identified five susceptibility loci. Four were at previously reported loci on 17q21, near IL1RL1, TSLP and IL33, but we report for the first time, to our knowledge, that these loci are associated with asthma risk in three ethnic groups. In addition, we identified a new asthma susceptibility locus at PYHIN1, with the association being specific to individuals of African descent (P = 3.9 × 10(-9)). These results suggest that some asthma susceptibility loci are robust to differences in ancestry when sufficiently large samples sizes are investigated, and that ancestry-specific associations also contribute to the complex genetic architecture of asthma

Evaluating the effectiveness of agricultural adaptation to climate change in preindustrial society

The effectiveness of agricultural adaptation determines the vulnerability of this sector to climate change, particularly during the preindustrial era. However, this effectiveness has rarely been quantitatively evaluated, specifically at a large spatial and long-term scale. The present study covers this case of preindustrial society in AD 1500–1800. Given the absence of technological innovations in this time frame, agricultural production was chiefly augmented by cultivating more land (land input) and increasing labor input per land unit (labor input). Accordingly, these two methods are quantitatively examined. Statistical results show that within the study scale, land input is a more effective approach of mitigating climatic impact than labor input. Nonetheless, these observations collectively improve Boserup's theory from the perspective of a large spatial and long-term scale.postprin

Characterizing the cancer genome in lung adenocarcinoma

Somatic alterations in cellular DNA underlie almost all human cancers(1). The prospect of targeted therapies(2) and the development of high-resolution, genome-wide approaches(3-8) are now spurring systematic efforts to characterize cancer genomes. Here we report a large-scale project to characterize copy-number alterations in primary lung adenocarcinomas. By analysis of a large collection of tumours ( n = 371) using dense single nucleotide polymorphism arrays, we identify a total of 57 significantly recurrent events. We find that 26 of 39 autosomal chromosome arms show consistent large-scale copy-number gain or loss, of which only a handful have been linked to a specific gene. We also identify 31 recurrent focal events, including 24 amplifications and 7 homozygous deletions. Only six of these focal events are currently associated with known mutations in lung carcinomas. The most common event, amplification of chromosome 14q13.3, is found in similar to 12% of samples. On the basis of genomic and functional analyses, we identify NKX2-1 ( NK2 homeobox 1, also called TITF1), which lies in the minimal 14q13.3 amplification interval and encodes a lineage-specific transcription factor, as a novel candidate proto-oncogene involved in a significant fraction of lung adenocarcinomas. More generally, our results indicate that many of the genes that are involved in lung adenocarcinoma remain to be discovered.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62944/1/nature06358.pd

The Fictional Character of Pornography

We refine a line of feminist criticism of pornography that focuses on pornographic works' pernicious effects. A.W. Eaton argues that inegalitarian pornography should be criticized because it is responsible for its consumers’ adoption of inegalitarian attitudes toward sex in the same way that other fictions are responsible for changes in their consumers’ attitudes. We argue that her argument can be improved with the recognition that different fictions can have different modes of persuasion. This is true of film and television: a satirical movie such as Dr. Strangelove does not morally educate in the same way as a realistic series such as The Wire. We argue that this is also true of pornography: inegalitarian depictions of sex are not invariably responsible for consumers' adoption of inegalitarian attitudes toward sex in reality. Given that pornographic works of different genres may harm in different ways, different feminist criticisms are appropriate for different genres of pornography

Somatic mutations affect key pathways in lung adenocarcinoma

Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well- classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers - including NF1, APC, RB1 and ATM - and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.National Human Genome Research InstituteWe thank A. Lash, M.F. Zakowski, M.G. Kris and V. Rusch for intellectual contributions, and many members of the Baylor Human Genome Sequencing Center, the Broad Institute of Harvard and MIT, and the Genome Center at Washington University for support. This work was funded by grants from the National Human Genome Research Institute to E.S.L., R.A.G. and R.K.W.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62885/1/nature07423.pd