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This paper reviews and synthesizes research into the ways in which parents support their child across three major developmental domains in early childhood: early language, play and early literacy. We show how these domains are linked to each other and suggest that there is some evidence that interventions in all of them will promote mutual development. Early interventions that focus on parent-child interactive experiences that are both routine and 'exotic' in nature are likely to be more powerful than practitioner-dominated interventions.

This study investigated the relationships between children's home literacy environments and their early hypotheses about printed words in the year prior to entering school. There were 147 children (70 girls and 77 boys: mean age 57 months, range = 47-66 months, standard deviation = 4.5 months) in the study. Results showed that the children had varying degrees of knowledge about printed words. Significant associations between age of the child and the application of hypotheses about printed words were found. In relation to the home literacy environments, parents with stronger literacy profiles and habits, whether to do with traditional forms of print or new techno-literacies, were more likely to read to their children on a daily basis, and these children were more likely to have developed hypotheses about the structure of printed words. The implications for understanding children's early literacy knowledge and relevance for educators of young children are discussed.

The notion that young children form and test hypotheses about early print is well established in relation to children from different cultures who use different languages. This study demonstrates that this also obtains for young deaf children still in the early stages of developing spoken language. Data collected from the homes of 13 deaf children (aged from 3 years 3 months to 4 years 4 months at the start of the study) over a two-year period showed hypothesising and experimenting around writing. Spontaneous drawing and writing samples were collected and a method of eliciting data was devised that did not rely on the children knowing vocabulary related to print (e.g. "word" or "sentence"). The data revealed that these children had internalised print concepts but this knowledge could easily be overlooked. Implications for educational settings are discussed. (Contains 6 tables and 5 figures.)

We sent questionnaires to families of all 288 children who had received cochlear implants at one center in the United Kingdom at least 5 years previously. Thus, it was a large, unselected group. We received 142 replies and 119 indicated that the child and family had changed their communication approach following cochlear implantation. In 113 cases the change was toward spoken language and in 6 cases the change was toward signed communication. Parents were asked to respond to statements about communication with their deaf child, and their responses indicated that parents wanted the most effective means of communication and one that their child would find most useful in the future. Findings that emerged from parents' comments indicated that the change toward greater use of spoken language was child-led and driven by increased audition. Parents also valued the contribution of signed communication.

Five cases of non-use of cochlear implants by children were investigated through semi-structured interviews with the children and their carers. The children were interviewed at school by a researcher who is deaf, and the carers, all of whom were hearing, were interviewed at home by a hearing researcher when the children were not present. The principal reason for non-use was found to be that the children disliked the sensation of sound provided by the implant, with some instances of pain and facial twitching reported. Some of the children were resistant to the idea of an implant from the outset and in all cases use was never fully established. Implications are drawn relating to selection, tuning and habilitation.

Background: Chronic glucocorticoid excess has been linked to increased atherosclerosis and general cardiovascular risk in humans. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) increases active glucocorticoid levels within tissues by catalyzing the conversion of cortisone to cortisol. Pharmacological inhibition of 11βHSD1 has been shown to reduce atherosclerosis in murine models. However, the cellular and molecular details for this effect have not been elucidated. Methodology/Principal Findings: To examine the role of 11βHSD1 in atherogenesis, 11βHSD1 knockout mice were created on the pro-atherogenic apoE−/− background. Following 14 weeks of Western diet, aortic cholesterol levels were reduced 50% in 11βHSD1−/−/apoE−/− mice vs. 11βHSD1+/+/apoE−/− mice without changes in plasma cholesterol. Aortic 7-ketocholesterol content was reduced 40% in 11βHSD1−/−/apoE−/− mice vs. control. In the aortic root, plaque size, necrotic core area and macrophage content were reduced ∼30% in 11βHSD1−/−/apoE−/− mice. Bone marrow transplantation from 11βHSD1−/−/apoE−/− mice into apoE−/− recipients reduced plaque area 39–46% in the thoracic aorta. In vivo foam cell formation was evaluated in thioglycollate-elicited peritoneal macrophages from 11βHSD1+/+/apoE−/− and 11βHSD1−/−/apoE−/− mice fed a Western diet for ∼5 weeks. Foam cell cholesterol levels were reduced 48% in 11βHSD1−/−/apoE−/− mice vs. control. Microarray profiling of peritoneal macrophages revealed differential expression of genes involved in inflammation, stress response and energy metabolism. Several toll-like receptors (TLRs) were downregulated in 11βHSD1−/−/apoE−/− mice including TLR 1, 3 and 4. Cytokine release from 11βHSD1−/−/apoE−/−-derived peritoneal foam cells was attenuated following challenge with oxidized LDL. Conclusions: These findings suggest that 11βHSD1 inhibition may have the potential to limit plaque development at the vessel wall and regulate foam cell formation independent of changes in plasma lipids. The diminished cytokine response to oxidized LDL stimulation is consistent with the reduction in TLR expression and suggests involvement of 11βHSD1 in modulating binding of pro-atherogenic TLR ligands. [ABSTRACT FROM AUTHOR]