British conchology : or, an account of the Mollusca which now inhabit the British Isles and the surrounding seas / by John Gwyn Jeffreys.

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British conchology : or, an account of the Mollusca which now inhabit the British Isles and the surrounding seas / by John Gwyn Jeffreys.

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British conchology : or, an account of the Mollusca which now inhabit the British Isles and the surrounding seas / by John Gwyn Jeffreys.

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Bromeliaceae do Herbário do Dr. Adolpho Lutz: Encholirium Lutzii L. B. Smith n. sp

Encholirium Lutzii is distinguished from the majority of species by its branched inflorescence. Only E. horridum L. B. Smith and rarely E. spectabile Martius exhibit this character, but have much larger flowers than E. Lutzii and stout floral axes. Also the wing of the seed in E. horridum is very long-caudate. We feel that it is particularly appropriate to dedicate this new species to Dr. Adolpho Lutz because of his great discoveries in the biological relationships of the Bromeliaceae.

Report of Lepocreadium Bimarium manter, 1940, Vitellibaculum Spinosa (Siddioi) & Cable, 1960) and Hirudinella Ventricosa (Pallas, 1774), parasites of marine fishes in Brazil

Lepocreadium bimarinum and Vitellibaculum spinosa are referred for the first time in Stephanolepis hispidus and in Brazil, and Hirudinella ventricosa is reported from Scomberomorus cavalla. Measurements, figures and comments are given.

Phenotypic consequences of copy number variation: insights from Smith-Magenis and Potocki-Lupski syndrome mouse models.

A large fraction of genome variation between individuals is comprised of submicroscopic copy number variation of genomic DNA segments. We assessed the relative contribution of structural changes and gene dosage alterations on phenotypic outcomes with mouse models of Smith-Magenis and Potocki-Lupski syndromes. We phenotyped mice with 1n (Deletion/+), 2n (+/+), 3n (Duplication/+), and balanced 2n compound heterozygous (Deletion/Duplication) copies of the same region. Parallel to the observations made in humans, such variation in gene copy number was sufficient to generate phenotypic consequences: in a number of cases diametrically opposing phenotypes were associated with gain versus loss of gene content. Surprisingly, some neurobehavioral traits were not rescued by restoration of the normal gene copy number. Transcriptome profiling showed that a highly significant propensity of transcriptional changes map to the engineered interval in the five assessed tissues. A statistically significant overrepresentation of the genes mapping to the entire length of the engineered chromosome was also found in the top-ranked differentially expressed genes in the mice containing rearranged chromosomes, regardless of the nature of the rearrangement, an observation robust across different cell lineages of the central nervous system. Our data indicate that a structural change at a given position of the human genome may affect not only locus and adjacent gene expression but also "genome regulation." Furthermore, structural change can cause the same perturbation in particular pathways regardless of gene dosage. Thus, the presence of a genomic structural change, as well as gene dosage imbalance, contributes to the ultimate phenotype.