162 resultados para Sinai
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par E. Andriveau ; gravé le trait et les montagnes par Gérin, les écritures par P. Rousset, les eaux par Mme Fontaine.
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Includes bibliographical references.
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Imperfect: map (Egypt and Sinai) in pocket wanting.
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Mount Ararat -- Mount Moriah -- Mount Sinai -- Mount Hor -- Mount Pisgah -- Mount Horeb -- Mount Carmel -- Mount Lebanon -- Mount Zion -- Mount Tabor -- Mount of Olives -- Mount Calvary -- The Mount of God.
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Parts 13,15 and 17 have each an index by Georg Friedrich Hermann Müller. No more published.
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Painting, Crusader, 13th century; 22-23/64 x 18-25/32 in. (center); 21-9/64 x 8-35/64 in. (each wing); tempera, gold and silver on wood
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Vols. 8-11 by Horace Hooker.
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Translation of: Biblical researches in Palestine, Mount Sinai and Arabia Petræa.
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Part I. To Mount Sinai.--Part II. Mount Sinai to Pisgah.
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pt. 1. Lower Egypt, with the Fayu͡m︡ and the Peninsula of Sinai.--pt. 2. Upper Egypt with Nubia as far as the Second Cataract and the Western Oases.
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t.2 Malte, Égypte, Nubie, Abyssini, Sinai.--t.3. Syrie, Palestine, comprenant le Sinaí, l'Arabie Pétrée et la Cilicie, par A. Chauvet et É. Isambert.
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At head of title: Dept. of Employment Security.
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"Lithoprinted."
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von Dr. Harry Torczyner
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Once thought rare, primary aldosteronism (PAL) is now reported to be responsible for 5–10% of hypertension. Unlike familial hyperaldosteronism type I (FH-I), FH-II is not glucocorticoidremediable and not associated with the hybrid CYP11B1/CYP11B2 gene mutation. At least five times more common than FH-I, FH-II is clinically indistinguishable from apparently sporadic PAL, suggesting an even higher incidence. Studies performed in collaboration with C Stratakis (NIH, Bethesda) on our largest Australian family (eight affected members) demonstrated linkage at chromosome 7p22. Linkage at this region was also found in a South American family (DNA provided by MI New, Mount Sinai School of Medicine, New York) and in a second Australian family. The combined multipoint LOD score for these 3 families is 4.61 (q = 0) with markers D7S462 and D7S517, providing strong support for this locus harbouring mutations responsible for FH-II. A newly identified recombination event in our largest Australian family has narrowed the region of linkage by 1.8 Mb, permitting exclusion of approximately half the genes residing in the originally reported 5 Mb linked locus. Candidate genes that are involved in cell cycle control are of interest as adrenal hyperplasia and adrenal adenomas are common in FH-II patients. A novel candidate gene in this linked region produces the retinoblastoma-associated Kruppel-associated box protein (RBaK) which interacts with the retinoblastoma gene product to repress the expression of genes activated by members of the E2F family of transcription factors.