Making the Digital Humanities More Open

BrailleSC will undertake its second stage of development by designing and deploying a WordPress-based accessibility tool that will create braille content for endusers who are blind or low vision. Specifically, we plan to extend the use of Anthologize--a free and open source plug-in for WordPress that currently translates any RSS text into PDF, ePub, HTML, or TEI--to include the conversion of text to braille. As a result, we will not only make it easy for content creators to convert a text into braille, thereby extending humanities content to hundreds of thousands of visually disabled readers, but we will also experiment with making braille available visually through the WordPress interface. In partnership with the Maryland Institute for Technology in the Humanities (MITH) at the University of Maryland, College Park, we will continue to model the ways in which digital humanities projects should be designed and implemented with the needs of disabled users in mind

Tumor Transcriptome Sequencing Reveals Allelic Expression Imbalances Associated with Copy Number Alterations

Due to growing throughput and shrinking cost, massively parallel sequencing is rapidly becoming an attractive alternative to microarrays for the genome-wide study of gene expression and copy number alterations in primary tumors. The sequencing of transcripts (RNA-Seq) should offer several advantages over microarray-based methods, including the ability to detect somatic mutations and accurately measure allele-specific expression. To investigate these advantages we have applied a novel, strand-specific RNA-Seq method to tumors and matched normal tissue from three patients with oral squamous cell carcinomas. Additionally, to better understand the genomic determinants of the gene expression changes observed, we have sequenced the tumor and normal genomes of one of these patients. We demonstrate here that our RNA-Seq method accurately measures allelic imbalance and that measurement on the genome-wide scale yields novel insights into cancer etiology. As expected, the set of genes differentially expressed in the tumors is enriched for cell adhesion and differentiation functions, but, unexpectedly, the set of allelically imbalanced genes is also enriched for these same cancer-related functions. By comparing the transcriptomic perturbations observed in one patient to his underlying normal and tumor genomes, we find that allelic imbalance in the tumor is associated with copy number mutations and that copy number mutations are, in turn, strongly associated with changes in transcript abundance. These results support a model in which allele-specific deletions and duplications drive allele-specific changes in gene expression in the developing tumor