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- Beral, V, et al.
(författare)
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Alcohol, tobacco and breast cancer - collaborative reanalysis of individual data from 53 epidemiological studies, including 58515 women with breast cancer and 95067 women without the disease
- 2002
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Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 1532-1827 .- 0007-0920. ; 87, s. 1234-45
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Tidskriftsartikel (refereegranskat)abstract
- Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58515 women with invasive breast cancer and 95067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19 - 1.45, P < 0.00001) for an intake of 35 - 44 g per day alcohol, and 1.46 (1.33 - 1.61, P < 0.00001) for greater than or equal to 45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1 % per 10 g per day, P < 0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22 255 women with breast cancer and 40 832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers= 1.03, 95% CI 0.98 - 1.07, and for current smokers=0.99, 0.92 - 1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver. (C) 2002 Cancer Research UK.
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| 3. |
- Haines, M M, et al.
(författare)
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The West London Schools Study : the effects of chronic aircraft noise exposure on child health
- 2001
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Ingår i: Psychological Medicine. - 0033-2917 .- 1469-8978. ; 31:8, s. 1385-1386
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Tidskriftsartikel (refereegranskat)abstract
- Background. Previous field studies have indicated that children's cognitive performance is impaired by chronic aircraft noise exposure. However, these studies have not been of sufficient size to account adequately for the role of confounding factors. The objective of this study was to test whether cognitive impairments and stress responses (catecholamines, cortisol and perceived stress) are attributable to aircraft noise exposure after adjustment for school and individual level confounding factors and to examine whether children exposed to high levels of social disadvantage are at greater risk of noise effects. Methods. The cognitive performance and health of 451 children aged 8-11 years, attending 10 schools in high aircraft noise areas (16 h outdoor Leq > 63 dBA) was compared with children attending 10 matched control schools exposed to lower levels of aircraft noise (16 h outdoor Leq < 57 dBA). Results. Noise exposure was associated with impaired reading on difficult items and raised annoyance, after adjustment for age, main language spoken and household deprivation. There was no variation in the size of the noise effects in vulnerable subgroups of children. High levels of noise exposure were not associated with impairments in mean reading score, memory and attention or stress responses. Aircraft noise was weakly associated with hyperactivity and psychological morbidity. Conclusions. Chronic noise exposure is associated with raised noise annoyance in children. The cognitive results indicate that chronic aircraft noise exposure does not always lead to generalized cognitive effects but, rather, more selective cognitive impairments on difficult cognitive tests in children.
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| 4. |
- Nordborg, M, et al.
(författare)
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The extent of linkage disequilibrium in Arabidopsis thaliana
- 2002
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 30:2, s. 190-193
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Tidskriftsartikel (refereegranskat)abstract
- Linkage disequilibrium (LD), the nonrandom occurrence of alleles in haplotypes, has long been of interest to population geneticists. Recently, the rapidly increasing availability of genomic polymorphism data has fueled interest in LD as a tool for fine-scale mapping, in particular for human disease loci(1). The chromosomal extent of LD is crucial in this context, because it determines how dense a map must be for associations to be detected and, conversely, limits how finely loci may be mapped(2). Arabidopsis thaliana is expected to harbor unusually extensive LD because of its high degree of selfing(3). Several polymorphism studies have found very strong LD within individual loci, but also evidence of some recombination(4-6). Here we investigate the pattern of LD on a genomic scale and show that in global samples, LD decays within approximately 1 cM, or 250 kb. We also show that LD in local populations may be much stronger than that of global populations, presumably as a result of founder events. The combination of a relatively high level of polymorphism and extensive haplotype structure bodes well for developing a genome-wide LD map in A. thaliana.
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| 5. |
- Addario-Berry, L, et al.
(författare)
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Ancestral maximum likelihood of evolutionary trees is hard
- 2004
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Ingår i: Journal of Bioinformatics and Computational Biology. - 0219-7200 .- 1757-6334. ; 2:2, s. 257-271
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Tidskriftsartikel (refereegranskat)abstract
- Maximum likelihood (ML) (Felsenstein, 1981) is an increasingly popular optimality criterion for selecting evolutionary trees. Finding optimal ML trees appears to be a very hard computational task - in particular, algorithms and heuristics for ML take longer to run than algorithms and heuristics for maximum parsimony (MP). However, while MP has been known to be NP-complete for over 20 years, no such hardness result has been obtained so far for ML. In this work we make a first step in this direction by proving that ancestral maximum likelihood (AML) is NP-complete. The input to this problem is a set of aligned sequences of equal length and the goal is to find a tree and an assignment of ancestral sequences for all of that tree's internal vertices such that the likelihood of generating both the ancestral and contemporary sequences is maximized. Our NP-hardness proof follows that for MP given in (Day, Johnson and Sankoff, 1986) in that we use the same reduction from VERTEX COVER; however, the proof of correctness for this reduction relative to AML is different and substantially more involved.
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