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Sökning: WFRF:(Le K. E.) > (2000-2004)

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1.
  • Adler, SS, et al. (författare)
  • Double helicity asymmetry in inclusive midrapidity pi(0) production for polarized p+p collisions at root s=200 GeV
  • 2004
  • Ingår i: Physical Review Letters. - 1079-7114. ; 93:20: 202002
  • Tidskriftsartikel (refereegranskat)abstract
    • We present a measurement of the double longitudinal spin asymmetry in inclusive pi(0) production in polarized proton-proton collisions at roots=200 GeV. The data were taken at the Relativistic Heavy Ion Collider with average beam polarizations of 0.27. The measurements are the first in a program to study the longitudinal spin structure of the proton, using strongly interacting probes, at collider energies. The asymmetry is presented for transverse momenta 1-5 GeV/c at midrapidity, where next-to-leading-order perturbative quantum chromodynamic (NLO pQCD) calculations well describe the unpolarized cross section. The observed asymmetry is small and is compared to a NLO pQCD calculation with a range of polarized gluon distributions.
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  • 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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  • Garte, S, et al. (författare)
  • Metabolic gene polymorphism frequencies in control populations
  • 2001
  • Ingår i: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. - 1055-9965. ; 10:12, s. 1239-1248
  • Tidskriftsartikel (refereegranskat)
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7.
  • Smits, KM, et al. (författare)
  • Association of metabolic gene polymorphisms with tobacco consumption in healthy controls
  • 2004
  • Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 110:2, s. 266-270
  • Tidskriftsartikel (refereegranskat)abstract
    • Polymorphisms in genes that encode for metabolic enzymes have been associated with variations in enzyme activity between individuals. Such variations could be associated with differences in individual exposure to carcinogens that are metabolized by these genes. In this study, we examine the association between polymorphisms in several metabolic genes and the consumption of tobacco in a large sample of healthy individuals. The database of the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens was used. All the individuals who were controls from the case-control studies included in the data set with information on smoking habits and on genetic polymorphisms were selected (n = 20,938). Sufficient information was available on the following genes that are involved in the metabolism of tobacco smoke constituents: CYPIAI, GSTMI, GSTTI, NAT2 and GSTPI. None of the tested genes was clearly associated with smoking behavior. Information on smoking dose, available for a subset of subjects, showed no effect of metabolic gene polymorphisms on the amount of smoking. No association between polymorphisms in the genes studied and tobacco consumption was observed; therefore, no effect of these genes on smoking behavior should be expected.
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  • Décréau, P.M.E. , Fergeau, P., Krasnosels'kikh, V., Le Guirriec, E., Lévêque , M., Martin, Ph. , Randriamboarison, O., Rauch, J. L., Sené, F. X., Séran, H. C., Trotignon, J.G. , Canu, P., Cornilleau, N., de Féraudy, H., Alleyne, H. , Yearby, K., Mögensen (författare)
  • Early results from the Whisper instrument on Cluster: an overview.
  • 2001
  • Ingår i: Annales Geophysicae. ; 19:10, s. . 1241-1258
  • Tidskriftsartikel (refereegranskat)abstract
    • The Whisper instrument yields two data sets: (i) the electron density determined via the relaxation sounder, and (ii) the spectrum of natural plasma emissions in the frequency band 2-80 kHz. Both data sets allow for the three-dimensional exploration of th
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  • Benhamou, S, et al. (författare)
  • Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk
  • 2002
  • Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 23:8, s. 1343-1350
  • Tidskriftsartikel (refereegranskat)abstract
    • Susceptibility to lung cancer may in part be attributable to inter-individual variability in metabolic activation or detoxification of tobacco carcinogens. The glutathione S-transferase M1 (GSTM1) genetic polymorphism has been extensively studied in this context; two recent meta-analyses of case-control studies suggested an association between GSTM1 deletion and lung cancer. At least 15 studies have been published after these overviews. We undertook a new meta-analysis to summarize the results of 43 published case-control studies including >18 000 individuals. A slight excess of risk of lung cancer for individuals with the GSTM1 null genotype was found (odds ratio (OR) = 1.17, 95% confidence interval (CI) 1.07-1.27). No evidence of publication bias was found (P = 0.4), however, it is not easy to estimate the extent of such bias and we cannot rule out some degree of publication bias in our results. A pooled analysis of the original data of about 9500 subjects involved in 21 case-control studies from the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens (GSEC) data set was performed to assess the role of GSTM1 genotype as a modifier of the effect of smoking on lung cancer risk with adequate power. Analyses revealed no evidence of increased risk of lung cancer among carriers of the GSTM1 null genotype (age-, gender- and center-adjusted OR = 1.08, 95% CI 0.98-1.18) and no evidence of interaction between GSTM1 genotype and either smoking status or cumulative tobacco consumption.
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  • Fynbo, H. O. U., et al. (författare)
  • New information on the beta-decay of Li-11 from Doppler broadened gamma lines
  • 2004
  • Ingår i: Nuclear Physics A. - : Elsevier BV. - 0375-9474. ; 736:1-2, s. 39-54
  • Tidskriftsartikel (refereegranskat)abstract
    • The gamma-ray spectrum following beta-decay of Li-11 has been remeasured at the ISOLDE facility at CERN. Two new transitions were observed through the use of large Ge-detectors. Most gamma-decays will follow beta-delayed neutron emission. Information on the energy of the neutron is derived from analysis of the gamma line-shape and used to construct a partial decay scheme for Li-11. Lifetime values for the 1(-) and 2(-) levels in Be-10 are also derived. A new partial decay scheme is presented. (C) 2004 Elsevier B.V. All rights reserved.
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19.
  • Gaurivaud, P., et al. (författare)
  • Variability of a glucose phosphotransferase system permease in Mycoplasma mycoides subsp mycoides Small Colony
  • 2004
  • Ingår i: Microbiology. - : Microbiology Society. - 1350-0872 .- 1465-2080. ; 150, s. 4009-4022
  • Tidskriftsartikel (refereegranskat)abstract
    • Intraclonal antigenic variation in pathogenic mycoplasma species is considered an important feature of host-pathogen interaction. Such intraclonal protein variation was observed for the interaction of Mycoplasma mycoides subsp. mycoides Small Colony, the agent of contagious bovine pleuropneumonia, with mAb 3F3. Colony immunostaining allows the definition of 3F3 ON- and 3F3 OFF-type variants, which revert at low frequency. Targets of mAb 3F3 were shown to be surface located, and resided on multiple polypeptides in the 58-68 kDa size range. Phage display and a genomic database were combined to determine the gene encoding the proteins recognized by mAb 3F3. A gene encoding the putative permease of the glucose phosphotransferase system was identified. Genome sequence analysis of strain PG1 revealed two highly similar copies of this gene, resulting from duplication of the chromosomal region carrying the gene. Southern blot analysis demonstrated the presence of this duplication in almost every African strain tested, but not in European strains. DNA analysis revealed that ON/OFF switching is governed by a base substitution occurring upstream of the coding region for the 3F3 epitope. This event generates a stop codon that results in the premature termination of the PtsG protein.
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  • Karlsson, Per Erik, 1957, et al. (författare)
  • New critical levels for ozone effects on young trees based on AOT40 and simulated cumulative leaf uptake of ozone
  • 2004
  • Ingår i: Atmospheric Environment. - : Elsevier BV. - 1352-2310. ; 38:15, s. 2283-2294
  • Tidskriftsartikel (refereegranskat)abstract
    • Leaf or needle ozone uptake was estimated for young trees at seven experimental sites across Europe using a stomatal conductance simulation model. Dose-response relationships based on cumulative leaf uptake of ozone (CUO) were calculated using different hourly ozone flux thresholds and these were compared to dose-response relationships based on daylight AOT40, which is currently used within the UNECE Convention on Long-Range Transboundary Air Pollution (CLRTAP). Regression analysis showed that the CUO-biomass response relationships were highly significant for both coniferous and broadleaf trees, and independent of which ozone flux threshold was applied. On the basis of this regressions analysis, an hourly flux threshold of 1.6 nmol m(-2) s(-1) (COO > 1.6) is proposed as the most appropriate for all species categories in deriving dose-response relationships. The analysis indicated that the current critical level for ozone impacts on European forests of AOT40 10 ppm h may not protect the most sensitive receptors and that critical levels for AOT40 and CUO > 1.6 of 5 ppm h and 4 mmol m(-2), respectively, are more appropriate. The research identified weaker dose-response relationships for the CUO exposure index compared with AOT40. Distinguishing between sensitive and less sensitive species substantially improved the CUO-biomass response relationships although, still, to a lesser extent than when exposure was expressed as AOT40. (C) 2004 Elsevier Ltd. All rights reserved.
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  • Oinonen, M., et al. (författare)
  • Non-analog beta decay of Rb-74
  • 2001
  • Ingår i: Physics Letters, Section B: Nuclear, Elementary Particle and High-Energy Physics. - 0370-2693. ; 511:2-4, s. 145-150
  • Tidskriftsartikel (refereegranskat)abstract
    • The magnitude of the Coulomb mixing parameter delta (l)(IM) has been experimentally deduced, for the first time, for the B decay of Rb-74. Th, estimated magnitude is derived from the feeding of the non-analog first excited 0(+) state in Kr-74. The inferred upper Limit of 0.07% is small compared to theoretical predictions. The half-life was measured to be 64.90(9) ms.
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  • Taioli, E, et al. (författare)
  • Polymorphisms in CYP1A1, GSTM1, GSTT1 and lung cancer below the age of 45 years
  • 2003
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 32:1, s. 60-63
  • Tidskriftsartikel (refereegranskat)abstract
    • Background A genetic component of early-onset lung cancer has been suggested. The role of metabolic gene polymorphisms has never been studied in young lung cancer cases. Phase 1 and Phase 2 gene polymorphisms are involved in tobacco carcinogens' metabolism and therefore in lung cancer risk. Methods The effect of metabolic gene polymorphisms on lung cancer at young ages was studied by pooling data from the Genetic Susceptibility to Environmental Carcinogens (GSEC) database. All primary lung cancer cases of both sexes who were Caucasian and less than or equal to45 years of age at diagnosis, and the corresponding controls were selected. We obtained 261 cases and 1452 controls. Results There was a marginally significant association between lung cancer and GST1 null genotype (OR = 1.2; 95% Cl: 1.0-1.6), and a significant association between lung cancer and the homozygous CYP1A1 Msp1 variant allele (CYP1A1*2A and *2B) genotype (OR = 4.7 95% Cl: 1.2-19.0). When data were stratified by smoking status, the association between CYP1A1 genotype and lung cancer was confined to never smokers. Conclusions These results suggest that metabolic genetic factors play a role in lung cancer developing at young ages.
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