Telelearning in health: a Canadian perspective.

OBJECTIVE: This project identified telelearning projects associated with the 13 established Canadian telehealth centers in order to describe the nature of their activities, outline enablers and barriers to these activities, and present key action plans to move the Canadian agenda on telelearning in health forward. MATERIALS AND METHODS: Data were collected by a one-page questionnaire sent to the Canadian telehealth centers. Recipients were asked to identify current partners in such activities and to indicate if such partners should complete a separate questionnaire. Forty-nine questionnaires were distributed. Reported enablers, barriers, and action plans were placed in categories and analyzed. Data from 37 questionnaires, referencing 101 projects, formed the basis of the analysis. RESULTS: More than half of the telelearning programs were developed for health providers, approximately one third for undergraduate or graduate students, and a small percentage for patients or the private sector. The most frequently used communication mode was two-way audio/video conferencing. Enabling conditions were grouped into four categories: Canada as a country, timing, infrastructure, and collaboration and support. Five categories of barriers were cited: lack of sustainable funding, insufficient infrastructure and resources for sustainable programs, absence of the required culture change, lack of standardization and defined policies, and unavailability of valid and reliable evaluation frameworks. Eight broad constructive action steps were suggested. CONCLUSIONS: The reported enablers can create momentum to carry telelearning into a position of prominence. The Canadian telehealth community recommends action steps that could facilitate the removal of barriers and maximize current opportunities.

Induction of genetic tandem duplications in Salmonella by polycyclic aromatic hydrocarbon and amine carcinogens.

6 polycyclic aromatic hydrocarbon or similar amine carcinogens were tested as inducers of genetic tandem duplications in a rough strain of Salmonella typhimurium. When metabolically activated by rat-liver microsomes, all 6 were active in inducing genetic tandem duplications, yielding from over 3 times to almost 14 times as many tandem duplicants per viable bacterium as did concurrent uninduced control cultures. These results extend the number and chemical diversity of carcinogens shown to induce genetic duplications in bacterial tester systems. We suggest that polycyclic hydrocarbon carcinogens may act in carcinogenesis by inducing genetic duplications or other genetic rearrangements. Duplication induction may be a useful genetic endpoint for screening potential carcinogens.

Lowered induction of genetic tandem duplications in Salmonella by the pKM101 plasmid.

Selection for 3-amino-1,2,4-triazole (AT) resistance in certain strains of Salmonella typhimurium has been previously shown to select for genetic tandem duplications of the histidine operon. We show here that agents which induce tandem duplications are less effective in such induction in the presence of the pKM101 plasmid. The presence of the plasmid also produces an increase in AT-resistance due to mechanisms other than duplication, presumably because pKM101 produces high levels of error-prone repair. We suggest that high levels of error-prone repair may cause decreases in tandem duplication induction and propose that error-prone repair and tandem duplication may be alternative cellular responses to certain DNA lesions.

Carcinogens induce genetic tandem duplications in Salmonella.

Extensive studies have shown that chemical carcinogenesis involves an initiation-promotion pattern. A gene amplification model of carcinogenesis predicts that initiation involves induction of a genetic tandem duplication. We use a system developed by Anderson and Roth to select for tandem duplication of the histidine operon of Salmonella typhimurium by selection for resistance to 3-amino-1,2,4-triazole. Evidence reported here shows that, consistent with prediction, 10 carcinogens are all active in inducing tandem duplications. Two toxic noncarcinogens show little or no activity under the conditions used in inducing tandem duplication but azide, a mutagenic noncarcinogen, did show some activity. 9 types of evidence now support the gene amplification initiation-promotion model of carcinogenesis.