63 resultados para sister mary joseph nodule


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J.W. Binns, Modern Language Review 101.2 (2006), 504-5:
‘This book is an important contribution to the study of Anglo-Latin poetry in the late seventeenth and early eighteenth centuries … ’Haan provides an able and authoritative account …, setting the poems in their contexts, and providing for each a very clear and penetrating analysis which traces the classical well-springs that lie behind much of Addison’s Latin writing, and also calls attention to non-traditional elements’.

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In 1943, the first description of familial idiopathic methemoglobinemia in the United Kingdom was reported in 2 members of one family. Five years later, Quentin Gibson (then of Queen's University, Belfast, Ireland) correctly identified the pathway involved in the reduction of methemoglobin in the family, thereby describing the first hereditary trait involving a specific enzyme deficiency. Recessive congenital methemoglobinemia (RCM) is caused by a deficiency of reduced nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase. One of the original propositi with the type 1 disorder has now been traced. He was found to be a compound heterozygote harboring 2 previously undescribed mutations in exon 9, a point mutation Gly873Ala predicting a Gly291Asp substitution, and a 3-bp in-frame deletion of codon 255 (GAG), predicting loss of glutamic acid. A brother and a surviving sister are heterozygous; each bears one of the mutations. Thirty-three different mutations have now been recorded for RCM. The original authors' optimism that RCM would provide material for future genetic studies has been amply justified.

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