A mother-child intervention program for adolescent mothers: Results from a randomized controlled trial (the TeeMo study).

Children of adolescent mothers are a high-risk group for negative child development. Previous findings suggest that early interventions may enhance child development by improving mother-child interaction. The purpose of the current study was to evaluate a mother-child intervention (STEEP-b) program in high-risk adolescent mother-infant dyads (N = 56) within a randomized controlled trial (RCT). Mother-child interaction was assessed at baseline (T1), postintervention (T2), and follow-up (T3). The primary outcome was the change in maternal sensitivity and child responsiveness from T1 to T2 that was measured by blinded ratings of videotaped mother-child-interaction with the Emotional Availability Scales. A modified intention-to-treat analysis was performed to examine the data. No intervention effect was found for maternal sensitivity, 95% CI [-0.59-0.60], p = .99, and child responsiveness, 95% CI [-0.51-0.62], p = .84. Maternal sensitivity and child responsiveness did not change over time in both groups (all ps > .05). A statistically nonsignificant, but potentially clinically meaningful difference emerged between rates of serious adverse events, SC: 4 (14.8%), STEEP-b: 1 (3.4%), possibly driven by different intensity of surveillance of dyads in the treatment groups. The current findings question the effectiveness of STEEP-b for high-risk adolescent mothers and do not justify the broad implementation of this approach.

Effects of multikinase inhibitors on pressure overload-induced right ventricular remodeling.

BACKGROUND: Little is known about the effects of current PAH therapies and receptor tyrosine kinase inhibitors on heart remodeling. We sought to investigate the effects of the multikinase inhibitors sunitinib (PDGFR-, VEGFR- and KIT-inhibitor) and sorafenib (raf1/b-, VEGFR-, PDGFR-inhibitor) on pressure overload induced right ventricular (RV) remodeling. METHODS: We investigated the effects of the kinase inhibitors on hemodynamics and remodeling in rats subjected either to monocrotaline (MCT)-induced PH or to surgical pulmonary artery banding (PAB). MCT rats were treated from days 21 to 35 with either vehicle, sunitinib (1mg/kg, 5mg/kg and 10mg/kg/day) or sorafenib (10mg/kg/day). PAB rats were treated with vehicle, sunitinib (10mg/kg/day) or sorafenib (10mg/kg/day) from days 7 to 21. RV function and remodeling were determined using echocardiography, invasive hemodynamic measurement and histomorphometry. RESULTS: Treatment with both sorafenib and sunitinib decreased right ventricular systolic pressure, pulmonary vascular remodeling, RV hypertrophy and fibrosis in MCT rats. This was associated with an improvement of RV function. Importantly, after PAB, both compounds reversed RV chamber and cellular hypertrophy, reduced RV interstitial and perivascular fibrosis, and improved RV function. CONCLUSION: We demonstrated that sunitinib and sorafenib reversed RV remodeling and significantly improved RV function measured via a range of invasive and non-invasive cardiopulmonary endpoints in experimental models of RV hypertrophy.