V ie liturgique et quotidienne a Carthage vers le milieu du lIJe siecle. Le témoignage de saint Cyprien et de ses contemporains d'Afrique [Reseña]

Reseña de VICTOR SAXER, "Vie liturgique et quotidienne a Carthage vers le milieu du lIJe siecle. Le témoignage de saint Cyprien et de ses contemporains d'Afrique", 1 vol. de 454 págs., Studi di antichita cristiana pubblicati a cura del Pontificio Istituto di Archeologia Cristiana, XXIX, Citta del Vaticano, 1969

Expansion of Canopy-Forming Willows Over the Twentieth Century on Herschel Island, Yukon Territory, Canada

Canopy-forming shrubs are reported to be increasing at sites around the circumpolar Arctic. Our results indicate expansion in canopy cover and height of willows on Herschel Island located at 70° north on the western Arctic coast of the Yukon Territory. We examined historic photographs, repeated vegetation surveys, and conducted monitoring of long-term plots and found evidence of increases of each of the dominant canopy-forming willow species (Salix richardsonii, Salix glauca and Salix pulchra), during the twentieth century. A simple model of patch initiation indicates that the majority of willow patches for each of these species became established between 1910 and 1960, with stem ages and maximum growth rates indicating that some patches could have established as late as the 1980s. Collectively, these results suggest that willow species are increasing in canopy cover and height on Herschel Island. We did not find evidence that expansion of willow patches is currently limited by herbivory, disease, or growing conditions. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s13280-011-0168-y) contains supplementary material, which is available to authorized users

A COL17A1 Splice-Altering Mutation Is Prevalent in Inherited Recurrent Corneal Erosions

PurposeCorneal dystrophies are a genetically heterogeneous group of disorders. We previously described a family with an autosomal dominant epithelial recurrent erosion dystrophy (ERED). We aimed to identify the underlying genetic cause of ERED in this family and 3 additional ERED families. We sought to characterize the potential function of the candidate genes using the human and zebrafish cornea.DesignCase series study of 4 white families with a similar ERED. An experimental study was performed on human and zebrafish tissue to examine the putative biological function of candidate genes.ParticipantsFour ERED families, including 28 affected and 17 unaffected individuals.MethodsHumanLinkage-12 arrays (Illumina, San Diego, CA) were used to genotype 17 family members. Next-generation exome sequencing was performed on an uncle–niece pair. Segregation of potential causative mutations was confirmed using Sanger sequencing. Protein expression was determined using immunohistochemistry in human and zebrafish cornea. Gene expression in zebrafish was assessed using whole-mount in situ hybridization. Morpholino-induced transient gene knockdown was performed in zebrafish embryos.Main Outcome MeasuresLinkage microarray, exome analysis, DNA sequence analysis, immunohistochemistry, in situ hybridization, and morpholino-induced genetic knockdown results.ResultsLinkage microarray analysis identified a candidate region on chromosome chr10:12,576,562–112,763,135, and exploration of exome sequencing data identified 8 putative pathogenic variants in this linkage region. Two variants segregated in 06NZ–TRB1 with ERED: COL17A1 c.3156C→T and DNAJC9 c.334G→A. The COL17A1 c.3156C→T variant segregated in all 4 ERED families. We showed biologically relevant expression of these proteins in human cornea. Both proteins are expressed in the cornea of zebrafish embryos and adults. Zebrafish lacking Col17a1a and Dnajc9 during development show no gross corneal phenotype.ConclusionsThe COL17A1 c.3156C→T variant is the likely causative mutation in our recurrent corneal erosion families, and its presence in 4 independent families suggests that it is prevalent in ERED. This same COL17A1 c.3156C→T variant recently was identified in a separate pedigree with ERED. Our study expands the phenotypic spectrum of COL17A1 disease from autosomal recessive epidermolysis bullosa to autosomal dominant ERED and identifies COL17A1 as a key protein in maintaining integrity of the corneal epithelium

Hans Wolter, Lyon I — Henri Holstein, Lyon II, collection Histoire des conciles œcuméniques, 1966

Munier Charles. Hans Wolter, Lyon I — Henri Holstein, Lyon II, collection Histoire des conciles œcuméniques, 1966. In: Revue des Sciences Religieuses, tome 42, fascicule 2, 1968. pp. 177-179