102 research outputs found

    Effects of Self-Pollination in the Genus Pinus

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    The problems of self-pollination among trees are a major concern to foresters. Silvicultural practices have an effect on the frequency of self-pollination.For example, a cut, such as a shelterwood or seed tree, reduces the number of individuals in the breeding population and increases the distance between individual trees. This tends to increase the frequency of self-pollination. These effects can either be helpful or harmful depending on the goals of the forester. Therefore, a basic understanding as to the effects of self-pollination on trees is necessary. The point of focus in this paper is the genus, Pinus. Self-pollination occurs naturally in the forests, but usually not to any great extent. Trees have phenological and morphological barriers to self-pollination that help reduce the frequency. When self-pollination does occur, recessive genes that may be carried in the heterozygous condition can be expressed. These can either cause various degrees of harmful changes or go unnoticed. Because only the lethal or deviant changes are highly observable, those are the ones associated with self-pollination. Therefore, self-pollination is generally thought of as being harmful. Self-pollination can also carry out an important function in the forest. When the environment changes, trees need to cope with that change. The variation carried in the genes of the population allow the species to adapt to environmental changes.A recessive gene that was once considered harmful can be necessary for the survival of the species. Self-pollination does have its place, but in the normal forest situation, outcrossing is the more common method of pollination

    Training the Mentor: Improving the Ability of Legal Experts to Teach Students and New Lawyers

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    Understanding the National Student Survey: investigations in languages, linguistics and area studies

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    This report is a summary of interviews and focus groups with around 100 students and 50 members of academic staff in departments of languages, linguistics or area studies at nine universities in the UK. In recent years, concerns have been expressed about the ambiguity of some of the statements which students are asked to respond to in the National Student Survey (NSS). This project set out to get a better understanding of how students and staff understand the questions. The interviews and focus groups were carried out by members of academic staff at the nine institutions who each then wrote an individual report of their findings. This summary is designed to enable wider distribution of these findings without identifying individual staff, institutions `or departments

    Conceptualising learning through simulation: An expansive approach forprofessional and personal learning

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    This paper explores different ways of conceptualising the learning that occurs as student nurses engage in simulation experiences. The conceptual frameworks discussed in this paper draw upon the work of Benner and Sutphen (2007) and Engeström (1994). Benner and Sutphen's work highlights the complex nature of situated knowledge in practice disciplines such as nursing. They suggest that knowledge must be constantly integrated within the curriculum through pedagogies of interpretation, formation, contextualisation and performance. These pedagogies present a framework, which may enhance our understanding of the impact of simulation upon student learning. Engeström's work on activity theory, recognises the links between learning and the environment of work and highlights the possibilities for learning to inspire change, innovation and the creation of new ideas. His notion of expansive learning offers nurse education a means of reconceptualising the learning that occurs during simulation. Together these frameworks present an opportunity for nurse education to articulate and theorise the learning inherent in simulation activities. © 2013 Elsevier Ltd

    Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

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    Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio

    Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

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    Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes
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