149 resultados para Willoughby


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Description of Edward Dell’s property in Willoughby which consists of part of Lot no.9. This includes a hand-drawn map and 1 ½ page handwritten description. The edges of this document are slightly burned. This does not affect the text, n.d.

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Letter to S.D. Woodruff regarding parts of Lots 9 and 10 in Willoughby and signed by Calvin Cudney and Ezekiel Cudney (2 copies). Both of these copies are slightly burned on the edges. This does not affect the text, Dec. 20, 1884.

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Diagram of lot no. 10 in Willoughby. The names on the outside of this document include: Matthew Singh, provincial land surveyor, Toronto; George S. Field, contractor, Niagara Falls; E. T. Phelps and H. Lyman, lawyer, Niagara Falls. The document is quite warn and fragile. This does not affect the text, n.d.

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Letter to P.I. Price asking him to make out a cheque in favour of German and Pettit for looking after certain petitions in Willoughby and Bertie Townships and in Welland. This is signed by H.H. Collier, March 5, 1906.

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With reproductions of original title-pages; head-pieces, initials, etc.

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With reproductions of original title-pages, head-pieces, initials, etc.

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Mode of access: Internet.

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Published in 1843 under title: Tradescant der Aeltere 1618 in Russland.

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Mode of access: Internet.

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Mode of access: Internet.

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To identify multiple sclerosis (MS) susceptibility loci, we conducted a genome-wide association study (GWAS) in 1,618 cases and used shared data for 3,413 controls. We performed replication in an independent set of 2,256 cases and 2,310 controls, for a total of 3,874 cases and 5,723 controls. We identified risk-associated SNPs on chromosome 12q13-14 (rs703842, P = 5.4 x 10(-11); rs10876994, P = 2.7 x 10(-10); rs12368653, P = 1.0 x 10(-7)) and upstream of CD40 on chromosome 20q13 (rs6074022, P = 1.3 x 10(-7); rs1569723, P = 2.9 x 10(-7)). Both loci are also associated with other autoimmune diseases. We also replicated several known MS associations (HLA-DR15, P = 7.0 x 10(-184); CD58, P = 9.6 x 10(-8); EVI5-RPL5, P = 2.5 x 10(-6); IL2RA, P = 7.4 x 10(-6); CLEC16A, P = 1.1 x 10(-4); IL7R, P = 1.3 x 10(-3); TYK2, P = 3.5 x 10(-3)) and observed a statistical interaction between SNPs in EVI5-RPL5 and HLA-DR15 (P = 0.001).

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Though difficult, the study of gene-environment interactions in multifactorial diseases is crucial for interpreting the relevance of non-heritable factors and prevents from overlooking genetic associations with small but measurable effects. We propose a "candidate interactome" (i.e. a group of genes whose products are known to physically interact with environmental factors that may be relevant for disease pathogenesis) analysis of genome-wide association data in multiple sclerosis. We looked for statistical enrichment of associations among interactomes that, at the current state of knowledge, may be representative of gene-environment interactions of potential, uncertain or unlikely relevance for multiple sclerosis pathogenesis: Epstein-Barr virus, human immunodeficiency virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, HHV8-Kaposi sarcoma, H1N1-influenza, JC virus, human innate immunity interactome for type I interferon, autoimmune regulator, vitamin D receptor, aryl hydrocarbon receptor and a panel of proteins targeted by 70 innate immune-modulating viral open reading frames from 30 viral species. Interactomes were either obtained from the literature or were manually curated. The P values of all single nucleotide polymorphism mapping to a given interactome were obtained from the last genome-wide association study of the International Multiple Sclerosis Genetics Consortium & the Wellcome Trust Case Control Consortium, 2. The interaction between genotype and Epstein Barr virus emerges as relevant for multiple sclerosis etiology. However, in line with recent data on the coexistence of common and unique strategies used by viruses to perturb the human molecular system, also other viruses have a similar potential, though probably less relevant in epidemiological terms. © 2013 Mechelli et al.