Usual Care for Clinicians, Unusual Care for Their Clients: Rearranging Priorities for Children’s Mental Health Services

Garland et al.’s comprehensive review of the state of clinic-based community-based mental health care for U.S. children highlights many recent advances in usual care (UC) while also describing the continued gap between need and service provision, the limited effectiveness of services provided, and a number of other obstructions and dilemmas ranging from perceived stigma on the part of families to limited fiscal resources on the part of service providers. Based on these long-standing concerns, the review summarizes research on three foci for change and offers future directions for each: Enhanced engagement strategies to retain families in services, improved training and support to increase the use of evidenced based practices, and expanded measurement and feedback systems to monitor services in real time. Unaddressed, however, is whether these changes are sufficient to reform children’s mental health care. Even if enacted extensively and outstandingly – a feat we imagine that nobody familiar with UC would realistically expect – will unmet need for care improve and effective services be available to the large number of children in need of mental health services

A regulatory pathway involving Notch1/β-catenin/Isl1 determines cardiac progenitor cell fate.

The regulation of multipotent cardiac progenitor cell (CPC) expansion and subsequent differentiation into cardiomyocytes, smooth muscle, or endothelial cells is a fundamental aspect of basic cardiovascular biology and cardiac regenerative medicine. However, the mechanisms governing these decisions remain unclear. Here, we show that Wnt/β-Catenin signaling, which promotes expansion of CPCs1–3, is negatively regulated by Notch1-mediated control of phosphorylated β-Catenin accumulation within CPCs, and that Notch1 activity in CPCs is required for their differentiation. Notch1 positively, and β-Catenin negatively, regulated expression of the cardiac transcription factors, Isl1, Myocd and Smyd1. Surprisingly, disruption of Isl1, normally expressed transiently in CPCs prior to their differentiation4, resulted in expansion of CPCs in vivo and in an embryonic stem (ES) cell system. Furthermore, Isl1 was required for CPC differentiation into cardiomyocyte and smooth muscle cells, but not endothelial cells. These findings reveal a regulatory network controlling CPC expansion and cell fate that involve unanticipated functions of β-Catenin, Notch1 and Isl1 that may be leveraged for regenerative approaches involving CPCs