Anatomia in qua tota humani corporis fabrica... Amstelodami, Ioannes Ianssonius, 1617

A paper affixed to the rear free endpaper of the item states that is edition contains “fine reproductions of the Gemini plates.” “Thomas Geminus was a a pseudonym for Thomas Lambrit, an engraver and printer…shown as active from about 1540; he died in May 1562.” http://www.arsanatomica.lib.ed.ac.uk/geminus.html accessed 11/20/2012. Geminus (Lambrit) printed Compendiosa totius anatomiae delineation aere exarata in 1545 copied from Vesalius’ 1543, De humani corporis fabrica . (Wellcome Library catalog, accessed 11/20/2012.) This book is a 1617 reproduction of the engraved copperplates which Lambrit himself copied from the original woodblock prints of the Vesalius’ book. Because the illustrations were based on those in the Vesalius’ book, because the name Vesalius helped sell the book, because copyright laws were not in effect, and because photocopies and digital images were not available, the author of this book is given as Andreas Vesalius. (Vesalius may or may not have been pleased.) For more information on Thomas Geminus (Lambrit) see The Anatomy of Thomas Geminus, by Geoffrey Keynes, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413790/?page=1

Transcriptional regulation of cell lineage-specific expression of the murine type I collagen genes and of osteoblast differentiation

The aim of my project is to examine the mechanisms of cell lineage-specific transcriptional regulation of the two type I collagen genes by characterizing critical cis-acting elements and trans-acting factors. I hypothesize that the transcription factors that are involved in the cell lineage-specific expression of these genes may have a larger essential role in cell lineage commitment and differentiation. I first examined the proximal promoters of the proα1(I) and the proα2(I) collagen genes for cell type-specific DNA-protein interactions, using in vitro DNaseI and in vivo DMS footprinting. These experiments demonstrated that the cis-acting elements in these promoters are accessible to ubiquitous DNA-binding proteins in fibroblasts that express these genes, but not in other cells that do not express these genes. I speculate that in type I collagen-expressing cells, cell type-specific enhancer elements facilitate binding of ubiquitous proteins to the proximal promoters of these genes. Subsequently, examination of the upstream promoter of the proα(I) collagen gene by transgenic mice experiments delineated a 117 bp sequence (-1656 to -1540 bp) as the minimum element required for osteoblast-specific expression. This 117 bp element contained two segments that appeared to have different functions: (1) the A-segment, which was necessary to obtain osteoblast-specific expression and (2) the C-segment, which was dispensable for osteoblast-specific expression, but was necessary to obtain high-level expression. In experiments to identify trans-acting factors that bind to the 117 bp element, I have demonstrated that the cell lineage-restricted homeodomain proteins, Dlx2, Dlx5 and mHOX, bound to the A-segment and that the ubiquitous transcription factor, Sp1, bound to the C-segment of this element. These results suggested a model where the binding of cell lineage-restricted proteins to the A-segment and of ubiquitous proteins to the C-segment of the 117 bp element of the proα1 (I) collagen gene activated this gene in osteoblasts. These results, combined with additional evidence that Dlx2, Dlx5 and mHOX are probably involved in osteoblast differentiation, support my hypothesis that the transcription factors involved in osteoblast-specific expression of type I collagen genes may have essential role in osteoblast lineage commitment and differentiation. ^