Effect of sieving on ex-situ soil respiration of soils from three land use types

This study aims to investigate the effect of sieving on ex situ soil respiration (CO2 flux) measurements from different land use types. We collected soils (0–10 cm) from arable, grassland and woodland sites, allocated them to either sieved (4-mm mesh, freshly sieved) or intact core treatments and incubated them in gas-tight jars for 40 days at 10 °C. Headspace gas was collected on days 1, 3, 17, 24, 31 and 38 and CO2 analysed. Our results showed that sieving (4 mm) did not significantly influence soil respiration measurements, probably because micro aggregates (< 0.25 mm) remain intact after sieving. However, soils collected from grassland soil released more CO2 compared with those collected from woodland and arable soils, irrespective of sieving treatments. The higher CO2 from grassland soil compared with woodland and arable soils was attributed to the differences in the water holding capacity and the quantity and stoichiometry of the organic matter between the three soils. We conclude that soils sieved prior to ex situ respiration experiments provide realistic respiration measurements. This finding lends support to soil scientists planning a sampling strategy that better represents the inhomogeneity of field conditions by pooling, homogenising and sieving samples, without fear of obtaining unrepresentative CO2 flux measurements caused by the disruption of soil architecture

March1-dependent modulation of donor MHC II on CD103+ dendritic cells mitigates alloimmunity.

In transplantation, donor dendritic cells (do-DCs) initiate the alloimmune response either by direct interaction with host T cells or by transferring intact donor MHC to host DCs. However, how do-DCs can be targeted for improving allograft survival is still unclear. Here we show CD103+ DCs are the major do-DC subset involved in the acute rejection of murine skin transplants. In the absence of CD103+ do-DCs, less donor MHC-II is carried to host lymph nodes, fewer allogenic T cells are primed and allograft survival is prolonged. Incubation of skin grafts with the anti-inflammatory mycobacterial protein DnaK reduces donor MHC-II on CD103+DCs and prolongs graft survival. This effect is mediated through IL-10-induced March1, which ubiquitinates and decreases MHC-II levels. Importantly, in vitro pre-treatment of human DCs with DnaK reduces their ability to prime alloreactive T cells. Our findings demonstrate a novel therapeutic approach to dampen alloimmunity by targeting donor MHC-II on CD103+DCs

The Role of Electron Captures in Chandrasekhar Mass Models for Type Ia Supernovae

The Chandrasekhar mass model for Type Ia Supernovae (SNe Ia) has received increasing support from recent comparisons of observations with light curve predictions and modeling of synthetic spectra. It explains SN Ia events via thermonuclear explosions of accreting white dwarfs in binary stellar systems, being caused by central carbon ignition when the white dwarf approaches the Chandrasekhar mass. As the electron gas in white dwarfs is degenerate, characterized by high Fermi energies for the high density regions in the center, electron capture on intermediate mass and Fe-group nuclei plays an important role in explosive burning. Electron capture affects the central electron fraction Y_e, which determines the composition of the ejecta from such explosions. Up to the present, astrophysical tabulations based on shell model matrix elements were only available for light nuclei in the sd-shell. Recently new Shell Model Monte Carlo (SMMC) and large-scale shell model diagonalization calculations have also been performed for pf-shell nuclei. These lead in general to a reduction of electron capture rates in comparison with previous, more phenomenological, approaches. Making use of these new shell model based rates, we present the first results for the composition of Fe-group nuclei produced in the central regions of SNe Ia and possible changes in the constraints on model parameters like ignition densities and burning front speeds.Comment: 26 pages, 8 figures, submitted to Ap

New Faces and New Masks of Today's Consumer

In 1995, we proposed that consumption and contemporary consumerism could not be studied or understood separately from the world of work and production. We proposed that contemporary consumerism was built on the back of what we referred to as `the Fordist Deal'. This deal, pioneered by Henry Ford for his employees, was the promise of ever increasing standards of living in exchange for a quiescent labour force accepting alienating work. Since that deal was struck, consumerism came to signify a general pre-occupation with consumption standards and choice as well as a willingness to read meanings in material commodities and to equate happiness and success with material possessions. In this sense, Ford may be seen as the father both of mass production and mass consumption. Since the Fordist high noon of consumerism in the West, mass consumption is widely seen as having fragmented into a proliferation of highly individualized niche products. For its part, a considerable part of mass production has migrated to countries with lower wages and looser environmental and social controls, fueling their own variants of consumerism. In this article, we examine the gradual erosion of the Fordist Deal in the light of developments in the last 10 years or so, seeking to assess the future of consumerism at a global level. We also seek to identify and discuss some emerging conceptualizations of the consumer, some of the new faces and masks assumed by the archetypal character of our types. We analyse some of the tensions and contradictions lurking behind these conceptualizations and try to envisage some of the real choices facing consumers today and some of the processes of social change that hinge on the outcomes of these choices. The article identifies a fundamental paradox between the ubiquity of the consumer in contemporary discourses and the virtual impossibility of generalizing about consumers. We suggest, then, that the consumer may be viewed as one of those `essentially contested concepts' proposed by Gallie that defy domestication. The consumer, we argue, is unmanageable, both as a concept, since no-one can pin it down to one specific conceptualization at the expense of all others, and as an entity, since attempts to control and manage the consumer lead to the consumer mutating from one impersonation to another. It is precisely this paradox that we seek to capture in our article's title. The article concludes with a consideration of three basic challenges that are liable to lead to fundamental reorientation of consumption and production, as well as of our conceptualizations and theorizing about them. These challenges are the outcomes of environmental, demographic and social factors that, we argue, make the current situation unsustainable and will bring about its dissolution

Association of MC1R Variants and host phenotypes with melanoma risk in CDKN2A mutation carriers: a GenoMEL study

&lt;p&gt;&lt;b&gt;Background&lt;/b&gt; Carrying the cyclin-dependent kinase inhibitor 2A (CDKN2A) germline mutations is associated with a high risk for melanoma. Penetrance of CDKN2A mutations is modified by pigmentation characteristics, nevus phenotypes, and some variants of the melanocortin-1 receptor gene (MC1R), which is known to have a role in the pigmentation process. However, investigation of the associations of both MC1R variants and host phenotypes with melanoma risk has been limited.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods&lt;/b&gt; We included 815 CDKN2A mutation carriers (473 affected, and 342 unaffected, with melanoma) from 186 families from 15 centers in Europe, North America, and Australia who participated in the Melanoma Genetics Consortium. In this family-based study, we assessed the associations of the four most frequent MC1R variants (V60L, V92M, R151C, and R160W) and the number of variants (1, &#8805;2 variants), alone or jointly with the host phenotypes (hair color, propensity to sunburn, and number of nevi), with melanoma risk in CDKN2A mutation carriers. These associations were estimated and tested using generalized estimating equations. All statistical tests were two-sided.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Results&lt;/b&gt; Carrying any one of the four most frequent MC1R variants (V60L, V92M, R151C, R160W) in CDKN2A mutation carriers was associated with a statistically significantly increased risk for melanoma across all continents (1.24 × 10−6 &#8804; P &#8804; .0007). A consistent pattern of increase in melanoma risk was also associated with increase in number of MC1R variants. The risk of melanoma associated with at least two MC1R variants was 2.6-fold higher than the risk associated with only one variant (odds ratio = 5.83 [95% confidence interval = 3.60 to 9.46] vs 2.25 [95% confidence interval = 1.44 to 3.52]; Ptrend = 1.86 × 10−8). The joint analysis of MC1R variants and host phenotypes showed statistically significant associations of melanoma risk, together with MC1R variants (.0001 &#8804; P &#8804; .04), hair color (.006 &#8804; P &#8804; .06), and number of nevi (6.9 × 10−6 &#8804; P &#8804; .02).&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusion&lt;/b&gt; Results show that MC1R variants, hair color, and number of nevi were jointly associated with melanoma risk in CDKN2A mutation carriers. This joint association may have important consequences for risk assessments in familial settings.&lt;/p&gt

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN