Promoting mental well-being among parents in the neonatal intensive care unit: a perspective on the role of Physician Associates.

Emotional disorders in parents of infants admitted to the neonatal intensive care unit (NICU) carry the potential for serious ramifications in neonatal and childhood outcomes. Despite this, current NICU mental health supports are less than optimum; postpartum mental health screening is limited, often missed in parents of inpatient infants, and may not be applicable to all family structures. Current evidence demonstrates improved outcomes in neonates and family members with early identification and multidisciplinary approaches to managing mental health problems. Physician Associates/Assistants (PAs) are a skilled group of advanced practice providers who are often a point of first contact for parents in the NICU, helping maintain continuity of care. In this perspective, we underscore leveraging the skills of PAs to promote the emotional wellbeing of parents in the NICU by way of practice and policy involvement. We also included a generic set of recommendations to equip PAs in this role.

Angiotensin II evokes angiogenic signals within skeletal muscle through co-ordinated effects on skeletal myocytes and endothelial cells.

Skeletal muscle overload induces the expression of angiogenic factors such as vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)-2, leading to new capillary growth. We found that the overload-induced increase in angiogenesis, as well as increases in VEGF, MMP-2 and MT1-MMP transcripts were abrogated in muscle VEGF KO mice, highlighting the critical role of myocyte-derived VEGF in controlling this process. The upstream mediators that contribute to overload-induced expression of VEGF have yet to be ascertained. We found that muscle overload increased angiotensinogen expression, a precursor of angiotensin (Ang) II, and that Ang II signaling played an important role in basal VEGF production in C2C12 cells. Furthermore, matrix-bound VEGF released from myoblasts induced the activation of endothelial cells, as evidenced by elevated endothelial cell phospho-p38 levels. We also found that exogenous Ang II elevates VEGF expression, as well as MMP-2 transcript levels in C2C12 myotubes. Interestingly, these responses also were observed in skeletal muscle endothelial cells in response to Ang II treatment, indicating that these cells also can respond directly to the stimulus. The involvement of Ang II in muscle overload-induced angiogenesis was assessed. We found that blockade of AT1R-dependent Ang II signaling using losartan did not attenuate capillary growth. Surprisingly, increased levels of VEGF protein were detected in overloaded muscle from losartan-treated rats. Similarly, we observed elevated VEGF production in cultured endothelial cells treated with losartan alone or in combination with Ang II. These studies conclusively establish the requirement for muscle derived VEGF in overload-induced angiogenesis and highlight a role for Ang II in basal VEGF production in skeletal muscle. However, while Ang II signaling is activated following overload and plays a role in muscle VEGF production, inhibition of this pathway is not sufficient to halt overload-induced angiogenesis, indicating that AT1-independent signals maintain VEGF production in losartan-treated muscle.