The behavioral and linguistic interactions of specifically language-delayed and normal boys with their mothers.

3 studies were based on subgroups selected from larger pools of either normal children or children with delays in the expression and/or comprehension of language but normal nonverbal abilities. In Study 1, younger (28-50 months) and older (51-68 months) normal (N = 27) and language-delayed (N = 33) boys were observed interacting with their mothers in free play and structured task situations. Although language-delayed children initiated fewer interactions, their responsiveness to maternal interactions, questions, and commands did not differ from that of normal children. Mothers questioned language-delayed children less frequently during tasks but did not differ from mothers of normal children on other measures of interaction, responsiveness, control, or reward strategies. In Study 2, the complexity of maternal speech directed to normal (N = 11) and expressively delayed (N = 11) boys who were matched on the basis of comprehensive skills did not differ. Maternal speech to boys with delays in both language expression and comprehension (N = 11) was significantly less complex. In Study 3, the discrepancy between the speech complexity of mothers and that of their language-delayed children (N = 47) was greatest in younger children with greater expression and comprehension delays, who initiated fewer interactions and proved less responsive to maternal interactions and questions.

Effects of chronic insulin and glucagon exposure on the biosynthesis of glycerolipids by cultured hepatocytes.

Primary cultures of adult rat hepatocytes incubated (24-72 h) in Waymouth's 752/1 medium, exhibited a marked decline (80-90%) in their ability to incorporate 0.5 mM [1,3-14C]glycerol and 1.0 mM palmitate into glycerolipids. The specific activities of glycerol kinase and sn-glycerol-3-P acyltransferase also showed a time-dependent reduction (30-80%). Phosphatidate phosphohydrolase, diacylglycerol cholinephosphotransferase, and fatty acid-CoA ligase activities were unaffected. Insulin and/or glucagon (10(-8) to 10(-6) M) not only prevented these reductions in hepatocyte monolayer glycerolipid formation and enzyme activities but increased (2-5-fold) the level of these processes. Cycloheximide (1 microM) reduced the insulin- and glucagon-dependent increases in sn-glycerol-3-P acyltransferase and glycerol kinase activity and glycerolipid biosynthesis. There was an excellent correlation (r greater than 0.93) between changes in glycerol kinase and sn-glycerol-3-P acyltransferase activity and the capacity of hepatocyte monolayers to incorporate labeled glycerol into glycerolipids under all conditions studied. Therefore, insulin and glucagon may regulate hepatic glycerolipid biosynthesis in part by maintaining the liver cell's enzymatic rate of glycerolipid biosynthesis.