Transcription factor ASCL2 is required for development of the glycogen trophoblast cell lineage.

The basic helix-loop-helix (bHLH) transcription factor ASCL2 plays essential roles in diploid multipotent trophoblast progenitors, intestinal stem cells, follicular T-helper cells, as well as during epidermal development and myogenesis. During early development, Ascl2 expression is regulated by genomic imprinting and only the maternally inherited allele is transcriptionally active in trophoblast. The paternal allele-specific silencing of Ascl2 requires expression of the long non-coding RNA Kcnq1ot1 in cis and the deposition of repressive histone marks.

A Dichotomy of Information-Seeking and Information-Trusting: Stem Cell Interventions and Children with Neurodevelopmental Disorders.

Parents and primary caregivers of children with Cerebral Palsy (CP) and Autism Spectrum Disorder (ASD) are faced with difficult treatment choices and management options for their children. The potential of stem cell technologies as an interventional strategy for CP and ASD has gained attention in the last decade. Information about these interventions varies in quality, resulting in a complex landscape for parent decision making for a child's care.

"You don't want to lose that trust that you've built with this patient...": (dis)trust, medical tourism, and the Canadian family physician-patient relationship.

Background: Recent trends document growth in medical tourism, the private pursuit of medical interventions abroad. Medical tourism introduces challenges to decision-making that impact and are impacted by the physician-patient trust relationship-a relationship on which the foundation of beneficent health care lies. The objective of the study is to examine the views of Canadian family physicians about the roles that trust plays in decision-making about medical tourism, and the impact of medical tourism on the therapeutic relationship.

Acute insulin signaling in pancreatic beta-cells is mediated by multiple Raf-1 dependent pathways.

Insulin enhances the proliferation and survival of pancreatic beta-cells, but its mechanisms remain unclear. We hypothesized that Raf-1, a kinase upstream of both ERK and Bad, might be a critical target of insulin in beta-cells. To test this hypothesis, we treated human and mouse islets as well as MIN6 beta-cells with multiple insulin concentrations and examined putative downstream targets using immunoblotting, immunoprecipitation, quantitative fluorescent imaging, and cell death assays.