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Sökning: WFRF:(Gallagher A) > (2000-2004)

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1.
  • Beral, V, et al. (författare)
  • 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
  • Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 1532-1827 .- 0007-0920. ; 87, s. 1234-45
  • 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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2.
  • Bower, K. N., et al. (författare)
  • ACE-2 HILLCLOUD. An overview of the ACE-2 ground-based cloud experiment
  • 2000
  • Ingår i: Tellus. Series B: Chemical and Physical Meteorology. - : Stockholm University Press. - 0280-6509. ; 52:2, s. 750-778
  • Tidskriftsartikel (refereegranskat)abstract
    • The ACE-2 HILLCLOUD experiment was carried out on the island of Tenerife in June-July 1997 to investigate the interaction of the boundary layer aerosol with a hill cap cloud forming over a ridge to the north-east of the island. The cloud was used as a natural flow through reactor to investigate the dependence of the cloud microphysics and chemistry on the characteristics of the aerosols and trace gases entering cloud, and to simultaneously study the influence of the physical and chemical processes occurring within the cloud on the size distribution, chemical and hygroscopic properties of the aerosol exiting cloud. 5 major ground base sites were used, measuring trace gases and aerosols upwind and downwind of the cloud, and cloud microphysics and chemistry and interstitial aerosol and gases within the cloud on the hill. 8 intensive measurement periods or runs were undertaken during cloud events, (nocturnally for seven of the eight runs) and were carried out in a wide range of airmass conditions from clean maritime to polluted continental. Polluted air was characterised by higher than average concentrations of ozone (> 50 ppbv), fine and accumulation mode aerosols (> 3000 and > 1500 cm -3 , respectively) and higher aerosol mass loadings. Cloud droplet number concentrations N, increased from 50 cm -3 in background maritime air to > 2500 cm -3 in aged polluted continental air, a concentration much higher than had previously been detected. Surprisingly, N was seen to vary almost linearly with aerosol number across this range. The droplet aerosol analyser (DAA) measured higher droplet numbers than the corrected forward scattering spectrometer probe (FSSP) in the most polluted air, but at other times there was good agreement (FSSP = 0.95 DAA with an r 2 = 0.89 for N < 1200 cm -3 ). Background ammonia gas concentrations were around 0.3 ppbv even in air originating over the ocean, another unexpected but important result for the region. NO 2 was present in background concentrations of typically 15 pptv to 100 pptv and NO 3 . (the nitrate radical) was observed at night throughout. Calculations suggest NO 3 . losses were mainly by reaction with DMS to produce nitric acid. Low concentrations of SO 2 (~30 pptv), HNO 3 and HCl were always present. HNO 3 concentrations were higher in polluted episodes and calculations implied that these exceeded those which could be accounted for by NO 2 oxidation. It is presumed that nitric and hydrochloric acids were present as a result of outgassing from aerosol, the HNO 3 from nitrate rich aerosol transported into the region from upwind of Tenerife, and HCl from sea salt aerosol newly formed at the sea surface. The oxidants hydrogen peroxide and ozone were abundant (i.e., were well in excess over SO 2 throughout the experiment). Occasions of significant aerosol growth following cloud processing were observed, particularly in cleaner cases. Observations and modelling suggested this was due mainly to the take up of nitric acid, hydrochloric acid and ammonia by the smallest activated aerosol particles. On a few occasions a small contribution was made by the in-cloud oxidation of S(IV). The implications of these results from HILLCLOUD for the climatologically more important stratocumulus Marine Boundary Layer (MBL) clouds are considered.
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  • Trappe, Scott, et al. (författare)
  • Human single muscle fibre function with 84 day bed-rest and resistance exercise.
  • 2004
  • Ingår i: Journal of physiology. - : Wiley. - 0022-3751. ; 557, s. 501-513
  • Tidskriftsartikel (refereegranskat)abstract
    • Muscle biopsies were obtained from the vastus lateralis before and after 84 days of bed-rest fromsix control (BR) and six resistance-exercised (BRE) men to examine slow- and fast-twitch muscle fibre contractile function. BR did not exercise during bed-rest and had a 17 and 40% decrease inwholemuscle size and function, respectively. TheBREgroup performedfour sets of seven maximal concentric and eccentric supine squats 2–3 days perweek (every third day) that maintained whole muscle strength and size. Slow (MHC I) and fast (MHC IIa) muscle fibres were studied at 15◦C for diameter, peak force (Po), contractile velocity (Vo) and force–power parameters. SDS-PAGE was performed on each single fibre after the functional experiments to determine MHC isoform composition. MHCI and IIa BR fibres were, respectively, 15 and 8% smaller, 46 and 25% weaker (Po), 21 and 6% slower (Vo), and 54 and 24% less powerful after bed-rest (P<0.05). BR MHCI and IIa Po and power normalized to cell size were lower (P<0.05). BRE MHCI fibres showed no change in size or Vo after bed-rest; however, Po was 19%lower (P<0.05), resulting in 20 and30%declines (P<0.05) in normalizedPo and power, respectively. BREMHCIIa fibres showed no change in size, Po and power after bed-rest, while Vo waselevated13%(P<0.05).BREMHCIIanormalizedPo andpowerwere10and15%lower (P<0.05), respectively.MHCisoformcomposition shifted away fromMHCI fibres, resulting in an increase (P<0.05) inMHCI/IIa (BR and BRE) andMHCIIa/IIx (BR only) fibres. These data show that the contractile function of the MHCI fibres was more affected by bed-rest and less influenced by the resistance exercise protocol than the MHCIIa fibres. Considering the large differences inpower ofhumanMHCIandIIamusclefibres (5- to6-fold), the maintenance of wholemuscle function with the resistance exercise programme is probably explained by (1) the maintenance of MHCIIa power and (2) the shift from slow to fast (MHC I→MHCI/IIa) in
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