998 resultados para John, Griffith, 1831-1912.


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Mode of access: Internet.

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Survey map and description of John Watson's land created by The Welland Canal Company. Included is a written description of the land along with a drawing of the land. The land totals 2 acres, 1 road, and 21 perches. The land was surveyed on September 5th, 1831.

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Mary Lyon -- Mrs. T.C. Doremus -- Fidelia Fiske -- Mrs. R.B. Lyth -- Ann Wilkins -- Mary Louisa Whately -- Melinda Rankin -- Lydia Mary Fay -- Mary Briscoe Baldwin -- Mrs. Bishop Gobat -- Miss Aldersey -- Mrs. H.C. Mullens -- Mrs. Bowen Thompson -- Miss Sophia Cooke -- Miss Charlotte Maria Tucker -- Miss Mary Reed -- Miss Fanny Jane Butler, M.D. -- Mrs. Emma V. Day -- Madame Coillard -- Mrs. Hannah Marshman -- Miss Harriet G. Brittan -- Mrs. John Geddie and Mrs. John Inglis -- Miss Louisa H. Anstey -- Miss Eliza Agnew -- Gertrude Egede -- Mrs. Murilla Baker Ingalls -- Miss Beulah Woolston -- Clara A. Swain, M.D.

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Mode of access: Internet.

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"This definitive edition of the dramatic works of St. John Hankin is limited to one thousand copies, of which nine hundred only are for sale in England and the United States of America. The type has been distributed."

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Bibliography: p. [215]-223.

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Introduction by C.J. Holmes.

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John Holling, a 1912 graduate of the University of Nebraska who died in 1988, established the "Peter and Anna Holling Fund" in 1973 with his sisters, Hattie and Elvena Holling, the only other surviving children at the time. Their siblings, Gustave, Emil, and Rose also had contributed to the estate. The Hollings were a pioneer farm family of German-Danish descent. Peter Holling settled in the Grand lsland area in the 1870s after missing a westbound Union Pacific work-train that he had originally boarded in Iowa.

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Mutations in the vacuolar–type H+-ATPase B1 subunit gene ATP6V1B1 cause autosomal–recessive distal renal tubular acidosis (dRTA). We previously identified a single-nucleotide polymorphism (SNP) in the human B1 subunit (c.481G.A; p.E161K) that causes greatly diminished pump function in vitro. To investigate the effect of this SNP on urinary acidification, we conducted a genotype-phenotype analysis of recurrent stone formers in theDallas and Bern kidney stone registries. Of 555 patients examined, 32 (5.8%) were heterozygous for the p.E161K SNP, and the remaining 523 (94.2%) carried two wild–type alleles. After adjustment for sex, age, body mass index, and dietary acid and alkali intake, p.E161K SNP carriers had a nonsignificant tendency to higher urinary pH on a random diet (6.31 versus 6.09; P=0.09). Under an instructed low–Ca and low–Na diet, urinary pH was higher in p.E161K SNP carriers (6.56 versus 6.01; P,0.01). Kidney stones of p.E161K carriers were more likely to contain calcium phosphate than stones of wild-type patients. In acute NH4Cl loading, p.E161K carriers displayed a higher trough urinary pH (5.34 versus 4.89; P=0.01) than wild-type patients. Overall, 14.6% of wild-type patients and 52.4% of p.E161K carriers were unable to acidify their urine below pH 5.3 and thus, can be considered to have incomplete dRTA. In summary, our data indicate that recurrent stone formers with the vacuolar H+-ATPase B1 subunit p.E161K SNP exhibit a urinary acidification deficit with an increased prevalence of calcium phosphate– containing kidney stones. The burden of E161K heterozygosity may be a forme fruste of dRTA.