The Origins of the Correlations between Tobacco, Alcohol, and Cannabis Use During Adolescence

Methods of structural equation modelling were used to analyse the correlations between reports of tobacco, alcohol, and cannabis use in a birth cohort of New Zealand children studied to the age of 16. This analysis produced three major conclusions: (a) the correlations between tobacco, alcohol, and cannabis use could be explained by a factor representing the individual's vulnerability to substance use; (b) predictors of vulnerability to substance use were the extent to which the individual affiliated with delinquent or substance using peers, novelty seeking, and parental illicit drug use; (c) in the region of 54% of the correlations between substance use behaviours could be predicted from observed risk factors and 46% was attributable to non-observed sources of vulnerability.     

Morbidity from 5 to 10 years

The prevalence and incidence of illness was examined in a birth cohort of Christchurch children studied during the age range of 5-10 years. At this age, children had an average of 12 consultations with family doctors; 26% were admitted to hospital and 53% made one or more attendances at hospital outpatient departments. The majority of general practitioner contacts involved five groups of conditions: respiratory illness; integumental lesion; accidents; gastrointestinal conditions; and hearing problems. Hospital admissions were dominated by five types of admission: respiratory illness; accidents; gastrointestinal conditions; genito-urinary problems; musculoskeletal problems. More than two-thirds of outpatient attendances were accounted for by accidents, respiratory illness, musculoskeletal problems, vision problems, and hearing problems. Trends in rates of medical consultation for accidents and respiratory illness during the period from birth to 10 years are described and the implications of the findings are discussed.     

Interleukin 18 inhibits osteoclast formation via T cell production of granulocyte macrophage colony-stimulating factor.

IL-18 inhibits osteoclast (OCL) formation in vitro independent of IFN-gamma production, and this was abolished by the addition of neutralizing antibodies to GM-CSF. We now establish that IL-18 was unable to inhibit OCL formation in cocultures using GM-CSF-deficient mice (GM-CSF -/-). Reciprocal cocultures using either wild-type osteoblasts with GM-CSF -/- spleen cells or GM-CSF -/- osteoblasts with wild-type spleen cells were examined. Wild-type spleen cells were required to elicit a response to IL-18 indicating that cells of splenic origin were the IL-18 target. As T cells comprise a large proportion of the spleen cell population, the role of T cells in osteoclastogenesis was examined. Total T cells were removed and repleted in various combinations. Addition of wild-type T cells to a GM-CSF -/- coculture restored IL-18 inhibition of osteoclastogenesis. Major subsets of T cells, CD4+ and CD8+, were also individually depleted. Addition of either CD4+ or CD8+ wild-type T cells restored IL-18 action in a GM-CSF -/- background, while IL-18 was ineffective when either CD4+ or CD8+ GM-CSF -/- T cells were added to a wild-type coculture. These results highlight the involvement of T cells in IL-18-induced OCL inhibition and provide evidence for a new OCL inhibitory pathway whereby IL-18 inhibits OCL formation due to action upon T cells promoting the release of GM-CSF, which in turn acts upon OCL precursors.     

Cognitive,educational, and behavioural outcomes at 7 to 8 years in a national very low birthweight cohort

AIMS—To examine cognitive, behavioural, and educational outcomes in middle childhood among a birth cohort of very low birthweight children.
METHODS—Two hundred and ninety eight survivors from a national birth cohort of 413 New Zealand very low birthweight (VLBW) children born in 1986 were assessed at 7 to 8 years of age on measures of behaviour, cognitive ability, school performance and the need for special education. These outcomes were compared with the same measures in a general population sample of over 1000 children studied at a similar age.
RESULTS—The VLBW children had significantly higher rates of problems and poorer levels of functioning across all outcome measures than the general child sample. These differences persisted even after control for variability in social, family, and other characteristics of the two samples and for the degree of sensorineural disability. There was evidence of a gradient of risk with birthweight, with extremely low birthweight children having generally higher rates of problems and difficulties than other VLBW children after covariate control.
CONCLUSIONS—The findings are consistent with a growing body of research evidence which suggests that premature and VLBW infants are at increased risk of longer term morbidity and functional impairment in middle childhood.