The Role of an Early Childhood Community Health Worker in Addressing Psycho-Social Needs in the Perinatal and Early Childhood Period.

OBJECTIVE: Addressing family psychosocial and mental health needs in the perinatal and early childhood period has a significant impact on long-term maternal and child health and is key to achieving health equity. We aimed to (1) describe and evaluate the role of an Early Childhood Community Health Worker (EC-CHW) to address psychosocial needs and improve psychosocial well-being for families in the perinatal period, and (2) examine factors associated with completion of goals. METHODS: An EC-CHW program was modeled after an existing hospital CHW program for children with special healthcare needs and chronic disease. An evaluation was conducted using repeated measures to assess improvements in psychosocial outcomes such as family stress and protective factors after participating in the EC-CHW program. Linear regression was also used to assess factors associated with completion of goals. RESULTS: Over a 21-month period (January 2019-September 2020), 161 families were referred to the EC-CHW. The most common reasons for referral included social needs and navigating systems for child developmental and behavioral concerns. There were high rates of family engagement in services (87%). After 6 months, families demonstrated statistically significant improvements in protective factors including positive parenting knowledge and social support. Only 1 key predictor variable, maternal depression, showed significant associations with completion of goals in the multivariable analysis. CONCLUSIONS: This study demonstrated the need for, and potential impact of an EC-CHW in addressing psychosocial and mental health needs in the perinatal period, and in a primary care setting. Impacts on protective factors are promising.

cGMP-dependent protein kinase-2 regulates bone mass and prevents diabetic bone loss.

NO/cGMP signaling is important for bone remodeling in response to mechanical and hormonal stimuli, but the downstream mediator(s) regulating skeletal homeostasis are incompletely defined. We generated transgenic mice expressing a partly-activated, mutant cGMP-dependent protein kinase type 2 (PKG2R242Q) under control of the osteoblast-specific Col1a1 promoter to characterize the role of PKG2 in post-natal bone formation. Primary osteoblasts from these mice showed a two- to three-fold increase in basal and total PKG2 activity; they proliferated faster and were resistant to apoptosis compared to cells from WT mice. Male Col1a1-Prkg2R242Q transgenic mice had increased osteoblast numbers, bone formation rates and Wnt/ß-catenin-related gene expression in bone and a higher trabecular bone mass compared to their WT littermates. Streptozotocin-induced type 1 diabetes suppressed bone formation and caused rapid bone loss in WT mice, but male transgenic mice were protected from these effects. Surprisingly, we found no significant difference in bone micro-architecture or Wnt/ß-catenin-related gene expression between female WT and transgenic mice; female mice of both genotypes showed higher systemic and osteoblastic NO/cGMP generation compared to their male counterparts, and a higher level of endogenous PKG2 activity may be responsible for masking effects of the PKG2R242Q transgene in females. Our data support sexual dimorphism in Wnt/ß-catenin signaling and PKG2 regulation of this crucial pathway in bone homeostasis. This work establishes PKG2 as a key regulator of osteoblast proliferation and post-natal bone formation.