Efficacy of the social-emotional learning foundations curriculum for kindergarten and first grade students at risk for emotional and behavioral disorders.

Researchers have shown that children's social-emotional growth is inextricably connected to academic learning. We developed the Social-Emotional Learning Foundations (SELF) intervention, a Grade K-1 curriculum merging social-emotional learning (SEL) and literacy instruction, to promote language supported self-regulation, specifically for primary grade children at early risk for emotional or behavioral difficulties. We report findings from a pretest-posttest cluster randomized efficacy trial with one fixed between-subjects factor to test the effects of teacher-delivered SEL instruction against those of business as usual (BAU). We recruited 163 kindergarten (K) and 141 first grade teachers from 52 schools across 11 school districts within one southeastern state. Our student sample (n = 1154) consisted of 627 kindergarteners and 527 first graders identified by teachers as at risk for internalizing or externalizing emotional and behavioral problems using the Systematic Screening for Behavioral Disorders; 613 of these students participated in the SELF condition and 541 participated in the BAU condition. We randomly assigned schools to SELF or BAU and used a multilevel model with three levels (i.e., children, classrooms, schools) to analyze data on subscales of six (four teacher-report and two direct) assessments related to self-regulation, social-emotional learning, social-emotional vocabulary, and general behavioral functioning. We found positive main effects of SELF compared to BAU on all but one measure, with effect sizes (calculated using Hedges' g) ranging from 0.20 to 0.65. Findings provide evidence for guiding future SEL intervention research and informing practice to improve student outcomes, particularly for children at risk for behavior problems.

Sodium deficiency and salt appetite in ICR: CD1 mice.

Using an outbred strain of mouse, we examined several characteristics of sodium appetite induced by depletion. We found that an appetite for 0.15 M NaCl solution was stimulated 24 h after injection of furosemide and access to a low-sodium diet, but not by low-sodium diet alone. When the duration of exposure to low-sodium diet was increased from 1 to 7 days, there was no additional effect on either the appetite or the blood plasma changes including elevated hematocrit ratio, protein and aldosterone concentrations, and plasma renin activity (PRA). Mice also showed an appetite for hypertonic (0.5 M) NaCl in solutions or in a gel matrix; the intakes of these two were comparable but the gel measurement was gravimetric so maybe more accurate. In the same study, we showed that single injections of either 10 or 40 mg/kg furosemide followed by a 24-h low-sodium diet produced similar appetites, but that 2.5 mg/kg had a submaximal effect. Lastly, we further validated the use of the gel matrix by showing in chronically depleted mice that intake was inversely related to NaCl concentration in the range 0.5-1.5 M, and that appetite was selective for sodium but not the anion with which it was paired.

Role of angiotensin in body fluid homeostasis of mice: effect of losartan on water and NaCl intakes.

It is known that mice injected peripherally with ANG II do not show a drinking response but that cFos immunoreactivity (ir) is induced in brain regions similar to those in rats. We now show in Crl:CD1(ICR) mice that peripheral injection of the ANG II type 1 receptor antagonist losartan was sufficient to prevent this induction of Fos-ir in the subfornical organ (SFO). Injection of ANG II into the lateral cerebral ventricle produced a robust water intake in mice and induced Fos-ir in SFO, as well as in median preoptic (MnPO) and paraventricular (PVN) nuclei. Peripheral injection of losartan blocked this drinking response and prevented the induction of Fos-ir in each of these brain regions. Hypovolemia produced by polyethylene glycol (PEG) produced a robust water intake but no evidence of sodium appetite, and it induced Fos-ir in SFO, MnPO, and PVN. Peripheral injection of losartan did not affect this drinking response. Fos-ir induced by PEG in SFO and MnPO was reduced by treatment with losartan, while that induced in the PVN was further increased by losartan. Sodium depletion with furosemide and low-sodium diet produced a strong sodium appetite and induced Fos-ir in SFO and MnPO. Treatment with losartan completely blocked the sodium appetite, as well as the induction of Fos-ir in these brain regions. These data indicate that endogenous production of ANG II and action at forebrain receptors is critically involved in depletion-related sodium appetite in mice. The absence of an effect of losartan on PEG-induced drinking suggests the critical involvement of other factor(s) such as arterial or venous baroreceptor input, and we discuss how this factor could also explain why peripheral ANG II is not dipsogenic in mice.