989 resultados para St. Clair, Arthur, 1734-1818.
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Mode of access: Internet.
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Mode of access: Internet.
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Mode of access: Internet.
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Caption on image includes title + Copyrighted by H.C. Hubel. St. Clair, Mich. 1910. On verso: Gift. Mr. Wifred Shaw. 12/15/1932 (Daybook, image #15)
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Back Row: Clarence Moulthrop, Lee Bonar, Julius St. Clair, Abraham Cohn, Charles Beath, William Cruse, Harold Rye, stud. mngr. Charles Boos
Middle Row: asst. coach Prentiss Douglas, asst. coach Robert Watson, Clifford Sparks, Chester Morrison, Lowell Genebach, Thomas Garrett, Archie Weston Harry Wellford, Gerald Froemke, Oscar Cartwright, trainer Harry Tuthill
Front Row: Oscar Lambert, Joseph Hanish, Alan Boyd, Elton Wieman, Angus Goetz, head coach Fielding Yost, John Goodsell, Richard Weske, William Fortune, Frank Culver
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Top Row: Grant Hicks, Roy Callahan, William Aubry, Stewart Hulse, John Groshko
3rd Row: Nathan Feinsinger Glen Rearick, Halbert Loomis, George Griffin, Edward Huggins
2nd row: Leonard Goldwater, Harold Cochran ,Clayton Purdy, James Brooker, Richard Freyberg, William DeHart Hubbard
Front Row: Richard Doyle, Charles Reinke, Coach Steve Farrell, captain W. Homer Hattendorf, st. mngr. Arthur Graves, Raymond Smith, William Roesser
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Crockett's attempt (ghost-written by Thomas Chilton) to correct erroneous impressions produced by Mathew St. Clair Clarke's The life and adventures of Colonel David Crockett of West Tennessee, which was published anonymously in 1833, and later reissued as Sketches and eccentricities of Colonel David Crockett of West Tennessee. Cf. introduction to the facsimile edition of the Narrative, edited by J.A. Shackford and S.J. Folmsbee, and published by the University of Tennessee Press.
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Mode of access: Internet.
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Mode of access: Internet.
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Mode of access: Internet.
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First published under title: Ante-Nicene Christian library, Edinburgh, 1867-97.
Control of cortex development by ULK4, a rare risk gene for mental disorders including schizophrenia
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This work was supported by the grants from British Council China (Sino-UK higher Education for PhD studies) to Y.D. and C.D.M., and also from the following funding resources: Tenovus Scotland (G12/05, B.L.), The Carnegie Trust (RG13060-10, B.L.) and National Natural Science Foundation of China (91232724, Y.D.; 31100788, L.Z.; 81200933, N.N.S.; 31528011, B.L. and Y.D.).
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Genome-wide association studies (GWAS) of schizophrenia have yielded more than 100 common susceptibility variants, and strongly support a substantial polygenic contribution of a large number of small allelic effects. It has been hypothesized that familial schizophrenia is largely a consequence of inherited rather than environmental factors. We investigated the extent to which familiality of schizophrenia is associated with enrichment for common risk variants detectable in a large GWAS. We analyzed single nucleotide polymorphism (SNP) data for cases reporting a family history of psychotic illness (N = 978), cases reporting no such family history (N = 4,503), and unscreened controls (N = 8,285) from the Psychiatric Genomics Consortium (PGC1) study of schizophrenia. We used a multinomial logistic regression approach with model-fitting to detect allelic effects specific to either family history subgroup. We also considered a polygenic model, in which we tested whether family history positive subjects carried more schizophrenia risk alleles than family history negative subjects, on average. Several individual SNPs attained suggestive but not genome-wide significant association with either family history subgroup. Comparison of genome-wide polygenic risk scores based on GWAS summary statistics indicated a significant enrichment for SNP effects among family history positive compared to family history negative cases (Nagelkerke's R(2 ) = 0.0021; P = 0.00331; P-value threshold <0.4). Estimates of variability in disease liability attributable to the aggregate effect of genome-wide SNPs were significantly greater for family history positive compared to family history negative cases (0.32 and 0.22, respectively; P = 0.031). We found suggestive evidence of allelic effects detectable in large GWAS of schizophrenia that might be specific to particular family history subgroups. However, consideration of a polygenic risk score indicated a significant enrichment among family history positive cases for common allelic effects. Familial illness might, therefore, represent a more heritable form of schizophrenia, as suggested by previous epidemiological studies.
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Lake sturgeon (Acipenser fulvescens) were historically abundant in the Huron-Erie Corridor (HEC), a 160 km river/channel network composed of the St. Clair River, Lake St. Clair, and the Detroit River that connects Lake Huron to Lake Erie. In the HEC, most natural lake sturgeon spawning substrates have been eliminated or degraded as a result of channelization and dredging. To address significant habitat loss in HEC, multi-agency restoration efforts are underway to restore spawning substrate by constructing artificial spawning reefs. The main objective of this study was to conduct post-construction monitoring of lake sturgeon egg deposition and larval emergence near two of these artificial reef projects; Fighting Island Reef in the Detroit River, and Middle Channel Spawning Reef in the lower St. Clair River. We also investigated seasonal and nightly timing of larval emergence, growth, and vertical distribution in the water column at these sites, and an additional site in the St. Clair River where lake sturgeon are known to spawn on a bed of ~100 year old coal clinkers. From 2010-12, we collected viable eggs and larvae at all three sites indicating that these artificial reefs are creating conditions suitable for egg deposition, fertilization, incubation, and larval emergence. The construction methods and materials, and physical site conditions present in HEC artificial reef projects can be used to inform future spawning habitat restoration or enhancement efforts. The results from this study have also identified the likelihood of additional uncharacterized natural spawning sites in the St. Clair River. In addition to the field study, we conducted a laboratory experiment involving actual substrate materials that have been used in artificial reef construction in this system. Although coal clinkers are chemically inert, some trace elements can be reincorporated with the clinker material during the combustion process. Since lake sturgeon eggs and larvae are developing in close proximity to this material, it is important to measure the concentration of potentially toxic trace elements. This study focused on arsenic, which occurs naturally in coal and can be toxic to fishes. Total arsenic concentration was measured in samples taken from four substrate treatments submerged in distilled water; limestone cobble, rinsed limestone cobble, coal clinker, and rinsed coal clinker. Samples were taken at three time intervals: 24 hours, 11 days, and 21 days. ICP-MS analysis showed that concentrations of total arsenic were below the EPA drinking water standard (10 ppb) for all samples. However, at the 24 hour sampling interval, a two way repeated measures ANOVA with a Holm-Sidak post hoc analysis (α= 0.05) showed that the mean arsenic concentration was significantly higher in the coal clinker substrate treatment then in the rinsed coal clinker treatment (p=0.006), the limestone cobble treatment (p