Risk-seeking and safety-seeking behaviours: a study of health-related behaviours among Norwegian school children

The purpose of this study was to investigate risk-seeking andsafety-seeking behaviours among schoolchildren in Norway. Behavioursthat give rise to a subjective experience of risk were labelledrisk seeking, and use of various kinds of safety equipment waslabelled safety seeking. The results yielded moderate to weak,but significant, inter-relationships between the various kindsof safety equipment. Factor analysis indicated that safety-seekingbehaviours and risk-seeking behaviours form two separate, althoughnegatively correlated, dimensions among the respondents. Thesedimensions seem to be part of more general health-related behaviourpatterns, previously labelled health-compromising and health-enhancinglifestyles. Our findings indicate that risk seeking and safetyseeking can be useful terms in the planning and developmentof health education programmes aimed at reducing accidents amongyoung people.     

Antibiotic resistance in Staphylococcus aureus colonising the intestines of Swedish infants

Staphylococcus aureus has become a frequent coloniser of the intestinal tract of infants, but the health effects of such colonisation are not clear. In this study, the antibiotic resistance patterns of 116 S. aureus strains from the commensal intestinal microflora were determined. The strains were obtained from 81 Swedish infants who had been followed with regular stool samples and registration of antibiotic usage during their first year of life. The faecal population levels of the individual strains and the duration of their persistence in the microflora had been determined previously. The prevalence of antibiotic resistance among the 116 strains was modest: methicillin, 0%; penicillin G, 78%; erythromycin A, 3%; tetracycline, 2%; clindamycin, 0.9%; and fusidic acid, 0.9%. Colonisation by antibiotic-resistant strains was unrelated to antibiotic consumption by individual infants. Antibiotic-resistant strains were as capable of persisting in the intestinal microflora and reaching high faecal population levels as fully susceptible strains. No strain lost or acquired resistance during the colonisation period. Thus, antibiotic-resistant strains of S. aureus seem to be as fit for competition in the large bowel microflora as susceptible strains, even in the absence of selective pressure from antibiotics. This may aggravate the ecological consequences of antibiotic resistance development.     

Upregulation of the Golgi protein GP73 by adenovirus infection requires the E1A CtBP interaction domain

GP73 is a novel type II Golgi transmembrane protein that is expressed at high levels in the hepatocytes of patients with viral hepatitis (R. D. Kladney, G. A. Bulla, L. Guo, A. L. Mason, A. E. Tollefson, D. J. Simon, Z. Koutoubi, and C. J. Fimmel, 2000, Gene 249, 53-65) and is induced in cultured cells by infection with viruses including adenoviruses. Its biological function and the mechanisms by which its expression may be regulated by viral infection are unknown. Here we report that GP73 is induced at the RNA and protein level in human Hep3B hepatoma cells infected by human Ad5 and Ad2. Hep3B cells were infected with wild-type or mutant adenoviruses. GP73 expression was measured by RNase protection assay, immunoblotting, or immunofluorescence microscopy. GP73 RNA and protein levels were strikingly induced following infection. The rise in GP73 expression coincided with the appearance of the adenovirus E1A and DBP proteins and preceded the expression of the fiber protein, a marker of the late phase of infection. Infection did not affect the expression of giantin, GPP130, or golgin-84, three integral Golgi membrane proteins with structural similarities to GP73. Mapping studies using a panel of mutant adenoviruses demonstrated that the E1A C-terminus, specifically its CtBP interaction domain (CID), is required for GP73 expression. Subsequently, Hep3B cells were transiently transfected with plasmids expressing wild-type or mutant E1A proteins. These studies confirmed that E1A induced GP73 expression via the CID. Our studies establish GP73 as a novel adenovirus-induced cellular protein whose expression is regulated through the CID of the E1A protein.     

Androgen receptor YAC transgenic mice carrying CAG 45 alleles show trinucleotide repeat instability

X-linked spinal and bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion in the first exon of the androgen receptor (AR) gene. Disease-associated alleles (37-66 CAGs) change in length when transmitted from parents to offspring, with a significantly greater tendency to shift size when inherited paternally. As transgenic mice carrying human AR cDNAs with 45 and 66 CAG repeats do not display repeat instability, we attempted to model trinucleotide repeat instability by generating transgenic mice with yeast artificial chromosomes (YACs) carrying AR CAG repeat expansions in their genomic context. Studies of independent lines of AR YAC transgenic mice with CAG 45 alleles reveal intergenerational instability at an overall rate of approximately 10%. We also find that the 45 CAG repeat tracts are significantly more unstable with maternal transmission and as the transmitting mother ages. Of all the CAG/CTG repeat transgenic mice produced to date the AR YAC CAG 45 mice are unstable with the smallest trinucleotide repeat mutations, suggesting that the length threshold for repeat instability in the mouse may be lowered by including the appropriate flanking human DNA sequences. By sequence-tagged site content analysis and long range mapping we determined that one unstable transgenic line has integrated an approximately 70 kb segment of the AR locus due to fragmentation of the AR YAC. Identification of the cis - acting elements that permit CAG tract instability and the trans -acting factors that modulate repeat instability in the AR YAC CAG 45 mice may provide insights into the molecular basis of trinucleotide repeat instability in humans.