Longitudinal tracking and retention in a school-based study on adolescent smoking: costs, variables, and smoking status.

Methods used to track a cohort of Grade 6 students through Grades 8 and 11, and costs involved for survey completion in school and by mail for ever and never smokers from the original group are detailed. At baseline, 1,598 students in Scarborough, Canada, completed a questionnaire on smoking, drinking, and health, and again in Grade 8 (N = 1,543/1,598) and Grade 11 (N = 1,454/1,598). In Grades 8 and 11, tracking and administering the questionnaire was more costly per participant when the survey was administered by mail than in school. Average completion costs were highest for Grade 11 students who used tobacco at baseline ($52.44). Students categorized as ever smokers in Grade 6 were harder to locate at each phase of testing, which suggests that this group should be identified at baseline so that closer tracking procedures may be employed between data collection points.

Genetic regulation of lipopolysaccharide-induced interleukin 1 production by murine peritoneal macrophages.

The production of IL 1 by LPS-stimulated peritoneal macrophages from inbred mouse strains was studied. Macrophages from A/J (A) mice were deficient in IL 1 production, when compared with high IL 1-producing strains, including C57BL/6J (B). The difference between A and B macrophages was maintained over a wide LPS concentration range and throughout a 72-hr incubation period. Because of these differences, it was possible to investigate the mechanisms regulating IL 1 production by applying techniques of genetic analysis by using recombinant inbred (RI) strains derived from the A and B progenitors. A strain distribution pattern (SDP) of IL 1 production (low/high response) was obtained with the use of 15 AXB/BXA RI strains. This suggested the presence of a major gene locus controlling the production of IL 1 in response to LPS stimulation, with allelic differences presumably resulting in deficient or efficient IL 1 production. In addition, there appeared to be one or more other loci involved in determining the magnitude of the IL 1 response to LPS in the responder mice. The IL 1 response did not appear to be linked to the major histocompatibility complex, since B10.A mice (which share the same H-2a haplotype as A/J) were efficient IL 1 producers. There did not appear to be any correlation between the degree of IL 1 production and the magnitude of the peritoneal macrophage inflammatory response, or between IL 1 production and LPS responsiveness (as determined by splenocyte proliferation). SDP analysis also indicated that the IL 1 response was not linked to macrophage tumoricidal activity. A comparison of the SDP for IL 1 production with a library of SDP for other known genetic waits suggested linkage with at least four loci on chromosome 1.