Sure Start graduates: predictors of attainment on starting school.

BACKGROUND: We report the analysis of the services used and the outcomes for children who used four Sure Start programmes prior to starting school in 2003. METHODS: A cohort study compared the intervention group both to classmates who lived in the areas covered by Sure Start but did not access it, and to a random sample of children in the same Local Education Authority who did not have access because they lived outside these areas. The impact of service use variables on various outcomes for users was explored using multiple linear regression analysis. RESULTS: No differences were found in school attainment between users and non-users on average. However, in one of the four areas, users' outcomes were consistently worse. By contrast, in one area, they appeared to be marginally superior on non-academic developmental scores. When we controlled for between-area differences, we also found an association between high use of Sure Start and personal and social development scores. IMPLICATIONS: Much of the variation in outcomes remains to be explained. Tentative findings suggest stronger associations between Sure Start use and better non-academic developmental outcomes. These findings add to our understanding of the impact of focused, high-quality pre-school provision. Methodological issues raised include rater bias, recruitment bias and a need to measure both frequency and type of service use.

The control of mitochondrial oxidations by complex III in rat muscle and liver mitochondria. Implications for our understanding of mitochondrial cytopathies in man.

We have studied the control by complex III of both succinate-cytochrome c reductase and of oxidative flux measured polarographically in rat muscle and liver mitochondria using the specific inhibitor, myxothiazol, to induce partial inhibitions of complex III activity. Complex III exerted a low degree of control on electron flux through succinate-cytochrome c reductase, and a 30-50% decrease in complex III activity remained undetected by this assay. However, when overall oxidative flux was measured polarographically there was a considerable difference in the effect of lowered complex III activity on this pathway between rat muscle and liver mitochondria. Small changes in complex III activity (approximately 5% inhibition) in muscle mitochondria caused marked changes in succinate-stimulated respiration, whereas in liver mitochondria complex III had to be inhibited by about 45% before changes in maximum oxidation rates could be detected. These differences between muscle and liver mitochondria occurred despite rat liver mitochondria having at least a 4-fold lower complex III activity. This suggests that when considering the biochemical consequences of defects of the respiratory chain an important factor is the degree to which an individual complex can be lowered before major changes in overall flux occur. In addition, since many patients with respiratory chain disease present with predominantly muscle symptoms, this latter finding suggests that an understanding of the control of mitochondrial oxidations by different tissues may be important when considering the tissue-specific nature of defects of the respiratory chain.