A comparison of matched and aggregated group outcomes data for evaluating continuing education of hematology and oncology health care professionals.

Introduction: Capturing educational outcomes from health care professionals is often challenging. Therefore, many providers utilize aggregated group data (comparing all preassessments to all postassessments) rather than matched group data (comparing pre- and postassessments only for those learners who completed both). To address the agreement between aggregate and matched outcomes, a preliminary analysis was conducted.

Loss of maternal CTCF is associated with peri-implantation lethality of Ctcf null embryos.

CTCF is a highly conserved, multifunctional zinc finger protein involved in critical aspects of gene regulation including transcription regulation, chromatin insulation, genomic imprinting, X-chromosome inactivation, and higher order chromatin organization. Such multifunctional properties of CTCF suggest an essential role in development. Indeed, a previous report on maternal depletion of CTCF suggested that CTCF is essential for pre-implantation development.

Derivation, characterization, and in vitro differentiation of canine embryonic stem cells.

Canine embryonic stem (cES) cell lines were generated to establish a large-animal preclinical model for testing the safety and efficacy of embryonic stem (ES) cell-derived tissue replacement therapy. Putative cES cell lines were initiated from canine blastocysts harvested from natural matings. Times of harvest were estimated as 12-16 days after the presumed surge in circulating levels of luteinizing hormone.

Inflammatory reactive oxygen species-mediated hemopoietic suppression in Fancc-deficient mice.

Patients with the genomic instability syndrome Fanconi anemia (FA) commonly develop progressive bone marrow (BM) failure and have a high risk of cancer. Certain manifestations of the disease suggest that the FA immune system is dysfunctional and may contribute to the pathogenesis of both BM failure and malignancies. In this study, we have investigated inflammation and innate immunity in FA hemopoietic cells using mice deficient in Fanconi complementation group C gene (Fancc).