480 research outputs found

    Spatial and temporal stability of weed patches in cereal fields under direct drilling and harrow tillage

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    The adoption of conservation agriculture (CA) techniques by farmers is changing the dynamics of weed communities in cereal fields and so potentially their spatial distribution. These changes can challenge the use of site-specific weed control, which is based on the accurate location of weed patches for spraying. We studied the effect of two types of CA (direct drilling and harrow-tilled to 20 cm) on weed patches in a three-year survey in four direct-drilled and three harrow-tilled commercial fields in Catalonia (North-eastern Spain). The area of the ground covered by weeds (hereafter called “weed cover”) was estimated at 96 to 122 points measured in each year in each field, in 50 cm × 50 cm quadrats placed in a 10 m × 10 m grid in spring. Bromus diandrus, Lolium rigidum, and Papaver rhoeas were the main weed species. The weed cover and degree of aggregation for all species varied both between and within fields, regardless of the kind of tillage. Under both forms of soil management all three were aggregated in elongated patterns in the direction of traffic. Bromus was generally more aggregated than Lolium, and both were more aggregated than Papaver. Patches were stable over time for only two harrow-tilled fields with Lolium and one direct-drilled field with Bromus, but not in the other fields. Spatial stability of the weeds was more pronounced in the direction of traffic. Herbicide applications, crop rotation, and traffic seem to affect weed populations strongly within fields, regardless of the soil management. We conclude that site-specific herbicides can be applied to control these species because they are aggregated, although the patches would have to be identified afresh in each season.This research was funded by the Spanish National Program (project: AGL2010-22084-C02-0). A.E.M. was funded by the Institute Strategic Programme (ISP) grants, “Soils to Nutrition” (S2N) grant number BBS/E/C/000I0330, and the joint Natural Environment Research Council (NERC) and Biotechnology and Biological Sciences Research Council (BBSRC) ISP grant “Achieving Sustainable Agricultural Systems” (ASSIST) grant number BBS/E/C/000I0100, using facilities funded by the BBSRC

    Early Ultraviolet, Optical and X-Ray Observations of the Type IIP SN 2005cs in M51 with Swift

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    We report early photospheric-phase observations of the Type IIP Supernova (SN) 2005cs obtained by Swift's Ultraviolet-Optical and X-Ray Telescopes. Observations started within two days of discovery and continued regularly for three weeks. During this time the V-band magnitude remained essentially constant, while the UV was initially bright but steadily faded until below the brightness of an underlying UV-bright HII region. This UV decay is similar to SNe II observed by the International Ultraviolet Explorer. UV grism spectra show the P-Cygni absorption of MgII 2798A, indicating a photospheric origin of the UV flux. Based on non-LTE model atmosphere calculations with the CMFGEN code, we associate the rapid evolution of the UV flux with the cooling of the ejecta, the peak of the spectral energy distribution (SED) shifting from ~700A on June 30th to ~1200A on July 5th. Furthermore, the corresponding recombination of the ejecta, e.g., the transition from FeIII to FeII, induces considerable strengthening of metal line-blanketing at and above the photosphere, blocking more effectively this fading UV flux. SN2005cs was not detected in X-rays, and the upper limit to the X-ray luminosity yields a limit to the mass loss rate of the progenitor of about 10^-5 solar masses per year. Overall, Swift presents a unique opportunity to capture the early and fast evolution of Type II SNe in the UV, providing additional constraints on the reddening, the SED shortward of 4000A, and the ionization state and temperature of the photon-decoupling regions.Comment: 15 pages, 6 figures. Accepted for publication by Astrophysical Journa

    Assessing interactions between the associations of common genetic susceptibility variants, reproductive history and body mass index with breast cancer risk in the breast cancer association consortium: a combined case-control study.

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    INTRODUCTION: Several common breast cancer genetic susceptibility variants have recently been identified. We aimed to determine how these variants combine with a subset of other known risk factors to influence breast cancer risk in white women of European ancestry using case-control studies participating in the Breast Cancer Association Consortium. METHODS: We evaluated two-way interactions between each of age at menarche, ever having had a live birth, number of live births, age at first birth and body mass index (BMI) and each of 12 single nucleotide polymorphisms (SNPs) (10q26-rs2981582 (FGFR2), 8q24-rs13281615, 11p15-rs3817198 (LSP1), 5q11-rs889312 (MAP3K1), 16q12-rs3803662 (TOX3), 2q35-rs13387042, 5p12-rs10941679 (MRPS30), 17q23-rs6504950 (COX11), 3p24-rs4973768 (SLC4A7), CASP8-rs17468277, TGFB1-rs1982073 and ESR1-rs3020314). Interactions were tested for by fitting logistic regression models including per-allele and linear trend main effects for SNPs and risk factors, respectively, and single-parameter interaction terms for linear departure from independent multiplicative effects. RESULTS: These analyses were applied to data for up to 26,349 invasive breast cancer cases and up to 32,208 controls from 21 case-control studies. No statistical evidence of interaction was observed beyond that expected by chance. Analyses were repeated using data from 11 population-based studies, and results were very similar. CONCLUSIONS: The relative risks for breast cancer associated with the common susceptibility variants identified to date do not appear to vary across women with different reproductive histories or body mass index (BMI). The assumption of multiplicative combined effects for these established genetic and other risk factors in risk prediction models appears justified.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

    BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

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    Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations

    tropiTree:an NGS-based EST-SSR resource for 24 tropical tree species

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    The development of genetic tools for non-model organisms has been hampered by cost, but advances in next-generation sequencing (NGS) have created new opportunities. In ecological research, this raises the prospect for developing molecular markers to simultaneously study important genetic processes such as gene flow in multiple non-model plant species within complex natural and anthropogenic landscapes. Here, we report the use of bar-coded multiplexed paired-end Illumina NGS for the de novo development of expressed sequence tag-derived simple sequence repeat (EST-SSR) markers at low cost for a range of 24 tree species. Each chosen tree species is important in complex tropical agroforestry systems where little is currently known about many genetic processes. An average of more than 5,000 EST-SSRs was identified for each of the 24 sequenced species, whereas prior to analysis 20 of the species had fewer than 100 nucleotide sequence citations. To make results available to potential users in a suitable format, we have developed an open-access, interactive online database, tropiTree (http://bioinf.hutton.ac.uk/tropiTree), which has a range of visualisation and search facilities, and which is a model for the efficient presentation and application of NGS data

    Common genetic variation in cellular transport genes and epithelial ovarian cancer (EOC) risk

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    Background Defective cellular transport processes can lead to aberrant accumulation of trace elements, iron, small molecules and hormones in the cell, which in turn may promote the formation of reactive oxygen species, promoting DNA damage and aberrant expression of key regulatory cancer genes. As DNA damage and uncontrolled proliferation are hallmarks of cancer, including epithelial ovarian cancer (EOC), we hypothesized that inherited variation in the cellular transport genes contributes to EOC risk. Methods In total, DNA samples were obtained from 14,525 case subjects with invasive EOC and from 23,447 controls from 43 sites in the Ovarian Cancer Association Consortium (OCAC). Two hundred seventy nine SNPs, representing 131 genes, were genotyped using an Illumina Infinium iSelect BeadChip as part of the Collaborative Oncological Gene-environment Study (COGS). SNP analyses were conducted using unconditional logistic regression under a log-additive model, and the FDR q<0.2 was applied to adjust for multiple comparisons. Results The most significant evidence of an association for all invasive cancers combined and for the serous subtype was observed for SNP rs17216603 in the iron transporter gene HEPH (invasive: OR = 0.85, P = 0.00026; serous: OR = 0.81, P = 0.00020); this SNP was also associated with the borderline/low malignant potential (LMP) tumors (P = 0.021). Other genes significantly associated with EOC histological subtypes (p<0.05) included the UGT1A (endometrioid), SLC25A45 (mucinous), SLC39A11 (low malignant potential), and SERPINA7 (clear cell carcinoma). In addition, 1785 SNPs in six genes (HEPH, MGST1, SERPINA, SLC25A45, SLC39A11 and UGT1A) were imputed from the 1000 Genomes Project and examined for association with INV EOC in white-European subjects. The most significant imputed SNP was rs117729793 in SLC39A11 (per allele, OR = 2.55, 95% CI = 1.5-4.35, p = 5.66x10-4). Conclusion These results, generated on a large cohort of women, revealed associations between inherited cellular transport gene variants and risk of EOC histologic subtypes
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