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Notes: Abstract: We investigated whether an increase in lumbar spine bone mineral density (LS BMD) at 6 months or at 12 months could predict the response to intermittent cyclical therapy (ICT) with etidronate, defined in one of two ways: (i) an increase in LS BMD at 24 months (improvement) or (ii) an increase in LS BMD ≥0.028 g/cm2 (significant improvement). The latter is a precision term calculated from test–retest values for LS BMD in osteoporotic patients. Two hundred and forty-seven patients (32 men; 5 premenopausal and 210 postmenopausal women) were followed for 24 months by dual-energy X-ray absorptiometry (DXA) and were not taking estrogen, calcitonin or fluoride during treatment with ICT-etidronate. One hundred and fifty patients had a LS BMD measurement after 6 months of treatment with ICT-etidronate and 205 patients had one at 12 months. Baseline characteristics (mean;SD) were as follows: age, 66;11 years; years since menopause, 21;10; number of vertebral fractures at baseline, 0.87;1.26; LS BMD T-score, −2.8;1.2. After 24 months of treatment with ICT-etidronate, 81% of the patients had an improvement, and 55% had a significant improvement at the LS. Only 6% significantly lost bone (loss of 0.028 g/cm2 or more). The mean percent change from baseline in LS BMD was 5.1% (95% confidence interval 4.2% to 6.0%). The results for men and postmenopausal women were similar to those for the entire group. Accuracy and sensitivity were marginally, but not significantly, higher when response was predicted using 12 month versus 6 month LS BMD measurements. The positive predictive values of improvement at 6 or 12 months were 89% and 90% respectively for improvement at 24 months, and 66% and 68% for significant improvement at 24 months. Identification of nonresponders was less successful and similar at 6 months and 12 months. Forty percent and 39% of the patients, who had no improvement at 6 or 12 months respectively, also had no improvement at 24 months, i.e., were true negatives, while 77% and 71% had no significant improvement at 24 months. The results may reflect slow response in a small subgroup of patients rather than nonresponse; however, no response at 1 year might identify patients whose rate of response is sufficiently slow that alternative therapy is justified. These data demonstrate a good response rate to ICT-etidronate and may help reduce the need for follow-up BMD measurements in those who show an early improvement.

Notes: Summary Herpes simplex virus type 2 is a human venereal pathogen which causes lethal neurological illness after intravaginal inoculation into BALB/cJ mice. In the present studies, we demonstrate that intravaginal vaccination with an attenuated strain of this virus, which possesses a partial deletion of the thymidine kinase gene, rapidly induced durable immunity to lethal intravaginal challenge with wild-type virus. Such immunity was characterized by a dramatic hyperplasia of genital lymph nodes and a significant reduction in wild-type virus replication and spread from the genital tract following lethal challenge. Of greater importance, immunity to lethal wild-type virus challenge in the genital tract was transferrable to non-immune mice with genital lymph node cells prepared 1 week after intravaginal vaccination but was not transferrable with serum or cells from other lymphoid organs tested at this time. The adoptive transfer of anti-viral immunity to wild-type challenge was also characterized by a diminution in wild-type virus replication and spread from the genital tract. These results suggest that an important component of cellular immunity to genital pathogens may be antigenic stimulation of genital lymph nodes.

Notes: Abstract Air pollution has been associated with adverse health effects. Difficulties in interpreting studies of health effects of exposure to air pollution arise in estimating exposure. Until recently, studies of effects of air pollution have relied on pollution exposure measurements obtained from fixed location air pollution stations monitoring outside air (to evaluate compliance with air quality standards, rather than to examine population exposure). However, recent evidence suggests that there are substantial differences between air pollution levels measured at such sites and levels to which people are actually exposed, i.e. ‘personal exposure’. The present study examines effects of ambient urban air pollution on persons suffering from asthma, healthy non-asthmatic subjects and school children (in 2 Canadian cities, Toronto and Hamilton). Air pollution exposure is being assessed by data obtained from: (1) conventional ‘abatement’ oriented fixed location air pollution monitoring stations, (2) an extensive ‘population’ oriented network, (3) inside and (4) outside structures (homes and schools) as well as (5) ‘personal’ air pollution samplers. The data indicate variability in these different estimates of exposure which have implications on health effects assessment.