Training Community Clergy in Serious Illness: Balancing Faith and Medicine.

Community-based clergy are highly engaged in helping seriously ill patients address spiritual concerns at the end of life (EOL). While they desire EOL training, no data exist in guiding how to conceptualize a clergy-training program. The objective of this study was used to identify best practices in an EOL training program for community clergy. As part of the National Clergy Project on End-of-Life Care, the project conducted key informant interviews and focus groups with active clergy in five US states (California, Illinois, Massachusetts, New York, and Texas). A diverse purposive sample of 35 active clergy representing pre-identified racial, educational, theological, and denominational categories hypothesized to be associated with more intensive utilization of medical care at the EOL. We assessed suggested curriculum structure and content for clergy EOL training through interviews and focus groups for the purpose of qualitative analysis. Thematic analysis identified key themes around curriculum structure, curriculum content, and issues of tension. Curriculum structure included ideas for targeting clergy as well as lay congregational leaders and found that clergy were open to combining resources from both religious and health-based institutions. Curriculum content included clergy desires for educational topics such as increasing their medical literacy and reviewing pastoral counseling approaches. Finally, clergy identified challenging barriers to EOL training needing to be openly discussed, including difficulties in collaborating with medical teams, surrounding issues of trust, the role of miracles, and caution of prognostication. Future EOL training is desired and needed for community-based clergy. In partnering together, religious-medical training programs should consider curricula sensitive toward structure, desired content, and perceived clergy tensions.

Health Care Chaplaincy: A Scoping Review of the Evidence 2009-2014.

There is a growing body of evidence investigating chaplaincy services. The purpose of this scoping review was to examine the empirical literature specific to the role of chaplaincy within health care published since 2009. Electronic searches of four databases were conducted in August 2015. After screening, 48 studies were retained and reviewed. Four themes emerged: experiences and perceptions of the health care chaplain (n = 15), chaplain practice (n = 9), emerging areas of health care chaplaincy (n = 16), and outcome studies (n = 8). Studies were diverse in topics covered, methods, national contexts, and clinical settings. The majority were descriptive in nature. Evidence continues to demonstrate a relationship between chaplains and increased patient satisfaction. Nascent areas of research include chaplain's role with diverse populations, involvement in clinical ethics, and confidence with research and evidence-based practice. Few conclusions can be drawn from the limited evidence on the outcomes of chaplain interventions.

Neural-specific inactivation of ShcA results in increased embryonic neural progenitor apoptosis and microencephaly.

Brain size is precisely regulated during development and involves coordination of neural progenitor cell proliferation, differentiation, and survival. The adapter protein ShcA transmits signals from receptor tyrosine kinases via MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) and PI3K (phosphatidylinositol 3-kinase)/Akt signaling pathways. In the CNS, ShcA expression is high during embryonic development but diminishes as cells differentiate and switches to ShcB/Sck/Sli and ShcC/N-Shc/Rai. To directly test ShcA function in brain development, we used Cre/lox technology to express a dominant-negative form of ShcA (ShcFFF) in nestin-expressing neural progenitors. ShcFFF-expressing mice display microencephaly with brain weights reduced to 50% of littermate controls throughout postnatal and adult life. The cerebrum appeared most severely affected, but the gross architecture of the brain is normal. Body weight was mildly affected with a delay in reaching mature weight. At a mechanistic level, the ShcFFF microencephaly phenotype appears to be primarily attributable to elevated apoptosis levels throughout the brain from embryonic day 10.5 (E10.5) to E12, which declined by E14.5. Apoptosis remained at normal basal levels throughout postnatal development. Proliferation indices were not significantly altered in the embryonic neuroepithelium or within the postnatal subventricular zone. In another approach with the same nestin-Cre transgene, conditional deletion of ShcA in mice with a homozygous floxed shc1 locus also showed a similar microencephaly phenotype. Together, these data suggest a critical role for ShcA in neural progenitor survival signaling and in regulating brain size.