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Träfflista för sökning "WFRF:(Axelson Olav 1937 ) "

Search: WFRF:(Axelson Olav 1937 )

  • Result 1-10 of 31
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1.
  • Ahmadi, Ahmad, 1964-, et al. (author)
  • GSTM1 and mEPHX polymorphisms in Parkinson's disease and age of onset
  • 2000
  • In: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier BV. - 0006-291X .- 1090-2104. ; 269:3, s. 676-680
  • Journal article (peer-reviewed)abstract
    • Both environmental and genetic factors are involved in the development of PD and biotransformation of exogenous and endogenous compounds and may play a role in inter-individual susceptibility. Therefore, we investigated the presence of null genotypes of GSTM1, GSTT1, and two polymorphisms of mEPHX in subjects with Parkinson's disease and in a reference population. The study included 35 male PD patients and a male control group including 283 subjects. Homozygosity of the histidine (H) 113 isoform of mEPHX was significantly increased in PD patients (odds ratio = 3.8 CI 95% 1.2–11.8) and analysis of allele frequencies displayed an increased frequency of the H-allele among PD patients (odds ratio = 1.9 CI 95% 1.1–3.3). However, a significantly elevated median age for the onset of PD was found among GSTM1 gene carriers (median age = 68 years) compared to PD patients being GSTM1 null genotypes (median age = 57 years). Our observations suggest that (H) 113 isoform of mEPHX, which has been suggested as a low activity isoform, is overrepresented in PD patients and that inherited carriers of the GSTM1 gene postpone the onset of PD. These detoxification pathways may represent important protective mechanisms against reactive intermediates modifying the susceptibility and onset of PD.
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2.
  • Axelson, Olav, 1937- (author)
  • Alternative for estimating the burden of lung cancer from occupational exposures - Some calculations based on data from Swedish men
  • 2002
  • In: Scandinavian Journal of Work, Environment and Health. - 0355-3140 .- 1795-990X. ; 28:1, s. 58-63
  • Journal article (peer-reviewed)abstract
    • Objectives. This study attempts to demonstrate a calculation of the occupational lung cancer burden using economically active men in Sweden as an example. Methods. Estimates were calculated using Swedish register data on occupation in 1970, lung cancer incidence in 1971-1989, smoking frequencies in 1963, and the formula I = RI0F + I0(I-F), where I is the overall incidence, R is the relative risk associated with a factor (here smoking), F is the fraction of persons at risk (smokers), and I0 is the incidence among those not at risk (nonsmokers). Results. Farmers, gardeners, forestry workers, and fishermen had the lowest lung cancer risk (42.1 per 100 000 person-years) and a smoking frequency of 44.7%. Their I0 was 12.6 or 8.4 per 100 000 person-years, taking R for smoking as 6 or 10, respectively. From these I0 estimates, the expected rates for white- and blue-collar workers (smoking frequencies 52.7 and 57.7%, respectively) were 45.8 and 49.1 per 100 000 person-years, as compared with the 22% and 57% higher observed rates, respectively. Weighing these excesses proportionally according to the sizes of the three occupational categories gave, respectively for R equal to 6 and 10, occupation-related excesses of 39% and 32% and population-attributable risks of 28% and 24%. Conclusions. About one-fourth of the lung cancers that occur among economically active Swedish men seem to have been related to occupation. This figure agrees with estimates made by other methods in Nordic countries. Due to interaction, the population-attributable risk from smoking is still high, 73% and 83% at relative risk values of 6 and 10, respectively.
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3.
  • Axelson, Olav, 1937-, et al. (author)
  • Assessing dose-response relationships by cumulative exposures in epidemiological studies
  • 2007
  • In: American Journal of Industrial Medicine. - : Wiley. - 0271-3586 .- 1097-0274. ; 50:3, s. 217-220
  • Journal article (peer-reviewed)abstract
    • Background: If the occurrence of disease monotonically increases with the degree of exposure in an epidemiologic study, a dose-response (or exposure-response) relationship is indicated and facilitates the interpretation that the exposure has a causal role. It is not uncommon, however, that there is some effect in terms of an overall increased relative risk but no clear dose-response relationship. Methods: Models presented here show that cumulative exposure, as involving the duration of exposure, is not an adequate parameter when more recent exposure or the intensity of the exposure plays the greater role for the disease outcome. Conclusions: In lack of a dose-response pattern by cumulative exposure, the interpretation of an overall increased risk might well be that there is no definite effect. The proper consideration should be, however, that the measure of exposure could be inadequate, suggesting a need for further analyses and evaluations of the material studied. © 2007 Wiley-Liss, Inc.
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4.
  • Axelson, Olav, 1937- (author)
  • Ethylene oxide and cancer
  • 2004
  • In: Occupational and Environmental Medicine. - 1351-0711 .- 1470-7926. ; 61
  • Journal article (peer-reviewed)
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5.
  • Axelson, Olav, 1937-, et al. (author)
  • Leukemia in childhood and adolescence and exposure to ionizing radiation in homes built from uranium-containing alum shale concrete
  • 2002
  • In: Epidemiology. - : Ovid Technologies (Wolters Kluwer Health). - 1044-3983 .- 1531-5487. ; 13:2, s. 146-150
  • Journal article (peer-reviewed)abstract
    • Concerns in Sweden about indoor radon around 1980 prompted measurements of gamma-radiation from the facades of houses to identify those constructed of uranium-containing alum shale concrete, with potentially high radon concentrations. To evaluate any possible risk of acute lymphocytic leukemia from exposure to elevated gamma-radiation in these homes, we identified the acute lymphocytic leukemia cases less than 20 years of age in Sweden during 1980-1989 as well as eight controls per case from the population registry, matching on age, gender, and county. Using the existing measurements, exposure was assessable for 312 cases and 1,418 controls from 151 properly measured municipalities. A conditional logistic odds ratio of 1.4 (95% confidence interval = 1.0-1.9) was obtained for those ever having lived in alum shale concrete houses, with the average exposure exceeding 0.10 microsieverts per hour. Comparing those who ever lived in alum shale concrete houses (divided by higher and lower annual average exposure) with those who never lived in such houses, we found a weak dose-response relation. The results suggest some risk of acute lymphocytic leukemia from indoor ionizing radiation among children and young adults.
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6.
  • Axelson, Olav, 1937-, et al. (author)
  • Multiple sclerosis and ionizing radiation.
  • 2001
  • In: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 120, s. 175-178
  • Journal article (peer-reviewed)abstract
    • The etiology of multiple sclerosis (MS) may involve exposure to infectious, chemical or physical agents damaging the blood-brain barrier and an autoimmune reaction against myelin breakdown products. Here we report a pooled analysis of 174 MS cases and 815 population controls from two case-control studies with regard to such a potentially damaging exposure, namely X-ray examinations, radiological work and treatment with ionizing radiation. Exposure was assessed by questionnaires to the subjects. We obtained odds ratios of 4.4 (95% confidence interval, CI, 1.6-11.6) and 1.8 (95% CI 1.2-2.6) for radiological work and X-ray examinations, respectively, 5 cases, but no controls, in one of the studies had been treated with ionizing radiation. Our data and some other observations reported in the literature suggest a contributory role for ionizing radiation to the development of MS in some cases.
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9.
  • Axelson, Olav, 1937-, et al. (author)
  • Regulatory toxicology and pharmacology.
  • 2003
  • In: International journal of occupational and environmental health. - 1077-3525 .- 2049-3967. ; 9, s. 386-389
  • Journal article (peer-reviewed)
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10.
  • Bochicchio, Francesco, et al. (author)
  • Residential radon exposure, diet and lung cancer : A case-control study in a Mediterranean region
  • 2005
  • In: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 114:6, s. 983-991
  • Journal article (peer-reviewed)abstract
    • We performed a case-control study in Lazio, a region in central Italy characterized by high levels of indoor radon, Mediterranean climate and diet. Cases (384) and controls (404) aged 35-90 years were recruited in the hospital. Detailed information regarding smoking, diet and other risk factors were collected by direct interview. Residential history during the 30-year period ending 5 years before enrolment was ascertained. In each dwelling, radon detectors were placed in both the main bedroom and the living room for 2 consecutive 6-month periods. We computed odds ratios (ORs) and 95% confidence intervals (CIs) for time-weighted radon concentrations using both categorical and continuous unconditional logistic regression analysis and adjusting for smoking, diet and other variables. Radon measurements were available from 89% and 91% of the time period for cases and controls, respectively. The adjusted ORs were 1.30 (1.03-1.64), 1.48 (1.08-2.02), 1.49 (0.82-2.71) and 2.89 (0.45-18.6) for 50-99, 100-199, 200-399 and 400+ Bq/m3, respectively, compared with 0-49 Bq/m3 (OR = 1, 0.56-1.79). The excess odds ratio (EOR) per 100 Bq/m3 was 0.14 (-0.11, 0.46) for all subjects, 0.24 (-0.09, 0.70) for subjects with complete radon measurements and 0.30 (-0.08, 0.82) for subjects who had lived in 1 or 2 dwellings. There was a tendency of higher risk estimates among subjects with low-medium consumption of dietary antioxidants (EOR = 0.32, -0.19, 1.16) and for adenocarcinoma, small cell and epidermoid cancers. This study indicates an association, although generally not statistically significant, between residential radon and lung cancer with both categorical and continuous analyses. Subjects with presumably lower uncertainty in the exposure assessment showed a higher risk. Dietary antioxidants may act as an effect modifier. © 2005 Wiley-Liss, Inc.
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