962 resultados para Henderson, Edward


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Memo to the warden and councilors for the County of Welland in council assembled regarding the contract of Edward Henderson. The terms of the contract have not been exceeded. This note is not signed, n.d.

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County of Welland estimate of work done on section no.1 of the tap drain at Marshville by Edward Henderson, signed by S.D. Woodruff. Estimate no.1, June, 1856.

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County of Welland estimate of work done on section no.1 and cleaning below the culvert of the tap drain at Marshville by Edward Henderson, signed by S.D. Woodruff. Estimate no.2, Oct., 1856.

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"Dr. Henderson visited the island as agent of the British and Foreign Bible Society ... His ... journal has furnished ... the materials for this volume." Cf. p. 5.

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The Making Connections: Innovations in Learning and Teaching Forum, jointly hosted by the Division of Technology, Information and Learning Support (TILS) and the Learning and Teaching Unit (LTU), was held on 20 June. The forum provided a snapshot of innovative practice across QUT, as well as an overview of services supporting innovation. Past events have attracted sizeable audiences and informal feedback has been very positive and encouraging. The objective of the forum is to give an opportunity to academic teaching staff to share their innovative practice with their peers, and it is planned that more events will be held to allow for further sharing of ideas. The program for the June 2012 forum included the following presentations: Ms Lindy Osborne: The 7pm Project Dr Ana Pavasovic: A multifaceted approach to teaching a first year unit Mr Paul Willis: Out of our comfort zone: How can Collaborate engage students in inclusive teaching practices Dr Kelly Zuniga: Can you draw what I see? Recasting the ‘crit’ to engage a larger classroom audience Dr Peter Bell, Dr Mark Lauchs, Amy Henderson and Edward Robinson: Crime Club: Lightbulb moments Dr Deboarh Peach: Improving student engagement through the integration of blended delivery approaches in WIL. Lindy Osborne Biography: As an early career academic, Lindy Osborne draws upon professional experience as a registered architect to offer students pioneering curricula that are firmly grounded in real-world practice. Since commencing her academic career in 2008, she has purposefully reconceptualised the delivery of Architectural Design, Technology, Professional Practice and Research subjects, using innovative digital technology and empowering students to direct their own learning. Lindy is cognisant of the impact that the physical learning environment has on students, and seeks to actively modify it to support students by enabling powerful enactive learning. Using technology embedded flexible learning spaces and innovative simulated office practice pedagogy,students actively learn in an authentic environment, redressing the structural and cyclical factors that have resulted in a lack of workplace learning opportunities. Lindy’s creative integration of interdisciplinary opportunities, popular culture, social media and Web-2.0 technologies connects with students on their level, while they develop critical professional skills both inside and perhaps more importantly outside, the formal classroom environment.

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The HOXB13 gene has been implicated in prostate cancer (PrCa) susceptibility. We performed a high resolution fine-mapping analysis to comprehensively evaluate the association between common genetic variation across the HOXB genetic locus at 17q21 and PrCa risk. This involved genotyping 700 SNPs using a custom Illumina iSelect array (iCOGS) followed by imputation of 3195 SNPs in 20,440 PrCa cases and 21,469 controls in The PRACTICAL consortium. We identified a cluster of highly correlated common variants situated within or closely upstream of HOXB13 that were significantly associated with PrCa risk, described by rs117576373 (OR 1.30, P = 2.62×10(-14)). Additional genotyping, conditional regression and haplotype analyses indicated that the newly identified common variants tag a rare, partially correlated coding variant in the HOXB13 gene (G84E, rs138213197), which has been identified recently as a moderate penetrance PrCa susceptibility allele. The potential for GWAS associations detected through common SNPs to be driven by rare causal variants with higher relative risks has long been proposed; however, to our knowledge this is the first experimental evidence for this phenomenon of synthetic association contributing to cancer susceptibility.

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Genome-wide association studies (GWAS) have identified 76 variants associated with prostate cancer risk predominantly in populations of European ancestry. To identify additional susceptibility loci for this common cancer, we conducted a meta-analysis of > 10 million SNPs in 43,303 prostate cancer cases and 43,737 controls from studies in populations of European, African, Japanese and Latino ancestry. Twenty-three new susceptibility loci were identified at association P < 5 × 10(-8); 15 variants were identified among men of European ancestry, 7 were identified in multi-ancestry analyses and 1 was associated with early-onset prostate cancer. These 23 variants, in combination with known prostate cancer risk variants, explain 33% of the familial risk for this disease in European-ancestry populations. These findings provide new regions for investigation into the pathogenesis of prostate cancer and demonstrate the usefulness of combining ancestrally diverse populations to discover risk loci for disease.

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Background Genome-wide association studies have identified multiple genetic variants associated with prostate cancer risk which explain a substantial proportion of familial relative risk. These variants can be used to stratify individuals by their risk of prostate cancer. Methods We genotyped 25 prostate cancer susceptibility loci in 40,414 individuals and derived a polygenic risk score (PRS).We estimated empirical odds ratios (OR) for prostate cancer associated with different risk strata defined by PRS and derived agespecific absolute risks of developing prostate cancer by PRS stratum and family history. Results The prostate cancer risk for men in the top 1% of the PRS distribution was 30.6 (95% CI, 16.4-57.3) fold compared with men in the bottom 1%, and 4.2 (95% CI, 3.2-5.5) fold compared with the median risk. The absolute risk of prostate cancer by age of 85 years was 65.8% for a man with family history in the top 1% of the PRS distribution, compared with 3.7% for a man in the bottom 1%. The PRS was only weakly correlated with serum PSA level (correlation = 0.09). Conclusions Risk profiling can identify men at substantially increased or reduced risk of prostate cancer. The effect size, measured by OR per unit PRS, was higher in men at younger ages and in men with family history of prostate cancer. Incorporating additional newly identified loci into a PRS should improve the predictive value of risk profiles. Impact:We demonstrate that the risk profiling based on SNPs can identify men at substantially increased or reduced risk that could have useful implications for targeted prevention and screening programs.

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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 region.

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Larschan family tree reaching back to 1815