Ariel - Volume 4 Number 6

Editors David A. Jacoby Eugenia Miller Tom Williams Associate Editors Paul Bialas Terry Burt Michael Leo Gail Tenikat Editor Emeritus and Business Manager Richard J. Bonnano Movie Editor Robert Breckenridge Staff Richard Blutstein Mary F. Buechler J.D. Kanofsky Rocket Weber David Maye

The developmental transcriptome for Lytechinus variegatus exhibits temporally punctuated gene expression changes

Embryonic development is arguably the most complex process an organism undergoes during its lifetime, and understanding this complexity is best approached with a systems-level perspective. The sea urchin has become a highly valuable model organism for understanding developmental specification, morphogenesis, and evolution. As a non-chordate deuterostome, the sea urchin occupies an important evolutionary niche between protostomes and vertebrates. Lytechinus variegatus (Lv) is an Atlantic species that has been well studied, and which has provided important insights into signal transduction, patterning, and morphogenetic changes during embryonic and larval development. The Pacific species, Strongylocentrotus purpuratus (Sp), is another well-studied sea urchin, particularly for gene regulatory networks (GRNs) and cis-regulatory analyses. A well-annotated genome and transcriptome for Sp are available, but similar resources have not been developed for Lv. Here, we provide an analysis of the Lv transcriptome at 11 timepoints during embryonic and larval development. Temporal analysis suggests that the gene regulatory networks that underlie specification are well-conserved among sea urchin species. We show that the major transitions in variation of embryonic transcription divide the developmental time series into four distinct, temporally sequential phases. Our work shows that sea urchin development occurs via sequential intervals of relatively stable gene expression states that are punctuated by abrupt transitions.National Science FoundationFirst author draf

Enhancing the role of case-oriented peer review to improve quality and safety in radiation oncology: Executive summary

AbstractThis report is part of a series of white papers commissioned for the American Society for Radiation Oncology (ASTRO) Board of Directors as part of ASTRO's Target Safely Campaign, focusing on the role of peer review as an important component of a broad safety/quality assurance (QA) program. Peer review is one of the most effective means for assuring the quality of qualitative, and potentially controversial, patient-specific decisions in radiation oncology. This report summarizes many of the areas throughout radiation therapy that may benefit from the application of peer review. Each radiation oncology facility should evaluate the issues raised and develop improved ways to apply the concept of peer review to its individual process and workflow. This might consist of a daily multidisciplinary (eg, physicians, dosimetrists, physicists, therapists) meeting to review patients being considered for, or undergoing planning for, radiation therapy (eg, intention to treat and target delineation), as well as meetings to review patients already under treatment (eg, adequacy of image guidance). This report is intended to clarify and broaden the understanding of radiation oncology professionals regarding the meaning, roles, benefits, and targets for peer review as a routine quality assurance tool. It is hoped that this work will be a catalyst for further investigation, development, and study of the efficacy of peer review techniques and how these efforts can help improve the safety and quality of our treatments

Enterocolitis induced by autoimmune targeting of enteric glial cells: A possible mechanism in Crohn's disease?

Early pathological manifestations of Crohn's disease (CD) include vascular disruption, T cell infiltration of nerve plexi, neuronal degeneration, and induction of T helper 1 cytokine responses. This study demonstrates that disruption of the enteric glial cell network in CD patients represents another early pathological feature that may be modeled after CD8(+) T cell-mediated autoimmune targeting of enteric glia in double transgenic mice. Mice expressing a viral neoself antigen in astrocytes and enteric glia were crossed with specific T cell receptor transgenic mice, resulting in apoptotic depletion of enteric glia to levels comparable in CD patients. Intestinal and mesenteric T cell infiltration, vasculitis, T helper 1 cytokine production, and fulminant bowel inflammation were characteristic hallmarks of disease progression. Immune-mediated damage to enteric glia therefore may participate in the initiation and/or the progression of human inflammatory bowel disease