8 research outputs found

    Reducing young driver crash casualties in Great Britain - Use of routine police crash data to estimate the potential benefits of graduated driver licensing

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    Crashes involving young drivers (YD) cause significant morbidity and mortality in Great Britain (GB). Graduated Driver Licensing (GDL) is used in some countries to address this. This study assessed potential casualty and cost savings of possible GDL programmes in GB. Police road crash data were analysed to identify YD crashes at night or while carrying passengers. These data were then used to estimate the potential effects of GDL. 314,561 casualties and 3469 fatalities occurred in YD crashes. 25.1% of YD crashes occurred between 9 pm and 6 am and 24.4% occurred with a 15- to 24-year old passenger in the car. A 'strict' form of GDL in GB (night time restriction 9 pm-6 am, no 15-24 year old passengers) with 50% compliance would prevent 114 deaths and 872 serious casualties each year. The estimated value of prevention is ÂŁ424M pa. A 'less strict' form of GDL (night time restriction 10 pm-5 am, maximum of one 15-19 year old passenger) with 50% compliance would prevent 81 deaths and 538 serious injuries. The estimated value of prevention is ÂŁ273M pa. Implementing GDL in GB could save significant numbers of lives. Public health organisations have a duty to advocate for such legislation

    The Utility of Routinely Collected Data in Evaluating Important Policy Changes: The New Zealand Alcohol Purchasing Age Limit Example

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    We used the recent lowering of the alcohol purchasing age in New Zealand to examine the proposition that routinely collected data are often insufficient in evaluating important policy changes. We estimated prechange and postchange incidence rate ratios for actual and hypothetical population sizes and hospital admissions related to alcohol poisoning and assaults. Even with a hypothetical youth population 10 times larger than New Zealand's actual youth population, comparisons were underpowered because there were too few observations. Governments should use the enactment of health legislation as an opportunity to build the research evidence base by ensuring that evaluations are initiated in advance

    Minimum purchasing age for alcohol and traffic crash injuries among 15-to 19-year-olds in New Zealand

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    Objectives: In 1999, New Zealand lowered the minimum purchasing age for alcohol from 20 to 18 years. We tested the hypothesis that this increased traffic crash injuries among 15- to 19-year-olds. Methods: Poisson regression was used to compute incidence rate ratios for the after to before incidence of alcohol-involved crashes and hospitalized injuries among 18- to 19-year-olds and 15- to 17-year-olds (20- to 24-year-olds were the reference). Results: Among young men, the ratio of the alcohol-involved crash rate after the law change to the period before was 12% larger (95% confidence interval [CI]=1.00, 1.25) for 18- to 19-year-olds and 14% larger (95% CI=1.01, 1.30) for 15- to 17-year-olds, relative to 20- to 24-year-olds. Among young women, the equivalent ratios were 51% larger (95% CI=1.17, 1.94) for 18- to 19-year-olds and 24% larger (95% CI=0.96, 1.59) for 15- to 17-year-olds. A similar pattern was observed for hospitalized injuries. Conclusions: Significantly more alcohol-involved crashes occurred among 15-to 19-year-olds than would have occurred had the purchase age not been reduced to 18 years. The effect size for 18- to 19-year-olds is remarkable given the legal exceptions to the pre-1999 law and its poor enforcement

    Common variants of the <i>BRCA1</i> wild-type allele modify the risk of breast cancer in <i>BRCA1</i> mutation carriers

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    Mutations in the &lt;i&gt;BRCA1&lt;/i&gt; gene substantially increase a woman's lifetime risk of breast cancer. However, there is great variation in this increase in risk with several genetic and non-genetic modifiers identified. The &lt;i&gt;BRCA1&lt;/i&gt; protein plays a central role in DNA repair, a mechanism that is particularly instrumental in safeguarding cells against tumorigenesis. We hypothesized that polymorphisms that alter the expression and/or function of &lt;i&gt;BRCA1&lt;/i&gt; carried on the wild-type (non-mutated) copy of the &lt;i&gt;BRCA1&lt;/i&gt; gene would modify the risk of breast cancer in carriers of &lt;i&gt;BRCA1&lt;/i&gt; mutations. A total of 9874 &lt;i&gt;BRCA1&lt;/i&gt; mutation carriers were available in the Consortium of Investigators of Modifiers of &lt;i&gt;BRCA1/2&lt;/i&gt; (CIMBA) for haplotype analyses of &lt;i&gt;BRCA1&lt;/i&gt;. Women carrying the rare allele of single nucleotide polymorphism rs16942 on the wild-type copy of &lt;i&gt;BRCA1&lt;/i&gt; were at decreased risk of breast cancer (hazard ratio 0.86, 95% confidence interval 0.77–0.95, &lt;i&gt;P&lt;/i&gt; = 0.003). Promoter &lt;i&gt;in vitro&lt;/i&gt; assays of the major &lt;i&gt;BRCA1&lt;/i&gt; haplotypes showed that common polymorphisms in the regulatory region alter its activity and that this effect may be attributed to the differential binding affinity of nuclear proteins. In conclusion, variants on the wild-type copy of &lt;i&gt;BRCA1&lt;/i&gt; modify risk of breast cancer among carriers of &lt;i&gt;BRCA1&lt;/i&gt; mutations, possibly by altering the efficiency of &lt;i&gt;BRCA1&lt;/i&gt; transcription
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