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Träfflista för sökning "WFRF:(Janzon R) srt2:(2005-2009)"

Search: WFRF:(Janzon R) > (2005-2009)

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  • Manuguerra, M., et al. (author)
  • Multi-factor dimensionality reduction applied to a large prospective investigation on gene-gene and gene-environment interactions
  • 2007
  • In: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 28:2, s. 414-422
  • Journal article (peer-reviewed)abstract
    • It is becoming increasingly evident that single-locus effects cannot explain complex multifactorial human diseases like cancer. We applied the multi-factor dimensionality reduction (MDR) method to a large cohort study on gene-environment and gene-gene interactions. The study (case-control nested in the EPIC cohort) was established to investigate molecular changes and genetic susceptibility in relation to air pollution and environmental tobacco smoke (ETS) in non-smokers. We have analyzed 757 controls and 409 cases with bladder cancer (n = 124), lung cancer (n = 116) and myeloid leukemia (n = 169). Thirty-six gene variants (DNA repair and metabolic genes) and three environmental exposure variables (measures of air pollution and ETS at home and at work) were analyzed. Interactions were assessed by prediction error percentage and cross-validation consistency (CVC) frequency. For lung cancer, the best model was given by a significant gene-environment association between the base excision repair (BER) XRCC1-Arg399Gln polymorphism, the double-strand break repair (DSBR) BRCA2-Asn372His polymorphism and the exposure variable 'distance from heavy traffic road', an indirect and robust indicator of air pollution (mean prediction error of 26%, P < 0.001, mean CVC of 6.60, P = 0.02). For bladder cancer, we found a significant 4-loci association between the BER APE1-Asp148Glu polymorphism, the DSBR RAD52-3'-untranslated region (3'-UTR) polymorphism and the metabolic gene polymorphisms COMT-Val158Met and MTHFR-677C > T (mean prediction error of 22%, P < 0.001, mean CVC consistency of 7.40, P < 0.037). For leukemia, a 3-loci model including RAD52-2259C > T, MnSOD-Ala9Val and CYP1A1-Ile462Val had a minimum prediction error of 31% (P < 0.001) and a maximum CVC of 4.40 (P = 0.086). The MDR method seems promising, because it provides a limited number of statistically stable interactions; however, the biological interpretation remains to be understood.
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3.
  • Vaissière, Thomas, et al. (author)
  • Quantitative analysis of DNA methylation after whole bisulfitome amplification of a minute amount of DNA from body fluids.
  • 2009
  • In: Epigenetics : official journal of the DNA Methylation Society. - 1559-2308. ; 4:4, s. 221-30
  • Journal article (peer-reviewed)abstract
    • Cell-free circulating DNA isolated from the plasma of individuals with cancer has been shown to harbor cancer-associated changes in DNA methylation, and thus it represents an attractive target for biomarker discovery. However, the reliable detection of DNA methylation changes in body fluids has proven to be technically challenging. Here we describe a novel combination of methods that allows quantitative and sensitive detection of DNA methylation in minute amounts of DNA present in body fluids (quantitative Methylation Analysis of Minute DNA amounts after whole Bisulfitome Amplification, qMAMBA). This method involves genome-wide amplification of bisulphite-modified DNA template followed by quantitative methylation detection using pyrosequencing and allows analysis of multiple genes from a small amount of starting DNA. To validate our method we used qMAMBA assays for four genes and LINE1 repetitive sequences combined with plasma DNA samples as a model system. qMAMBA offered high efficacy in the analysis of methylation levels and patterns in plasma samples with extremely small amounts of DNA and low concentrations of methylated alleles. Therefore, qMAMBA will facilitate methylation studies aiming to discover epigenetic biomarkers, and should prove particularly valuable in profiling a large sample series of body fluids from molecular epidemiology studies as well as in tracking disease in early diagnostics.
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4.
  • Janzon, Bo, et al. (author)
  • The Future of Warheads, Armour and Ballistics
  • 2007
  • In: Proceedings, 23rd International Symposium on Ballistics, Tarragona, Spain, 2007, ISBN 978-84-7493-379-6.
  • Conference paper (peer-reviewed)abstract
    • In 1983 a “Grand Old Man” of Ballistic Science, Dr. Robert J. Eichelberger, wrote1 : ”Ballistic technology is generally considered a mature technology – as it should be after centuries of intensive attention of some of the finest scientific minds of the world.” He predicted that increased understanding of relevant physics and chemistry and development of mathematical techniques and computer models would be key elements in the future of ballistics and weapon system design. These predictions were very accurate! But to-day’s developments and those of the foreseeable future go beyond this. Warheads and ballistics – interior, exterior and terminal – are very dependent on the use and properties of energetic materials – propellants and explosives – for their functioning. New, potentially very powerful substances such as the N5+ and N5– ions and metallic hydrogen were created in labs. Air-breathing propulsion – ramjets etc. - and efficient use of the high combustion energy of some metals adds to the performance increase potential. Increased use of intelligence, computers, sensors and fuzing in weapons, munitions and armours has added another dimension to the efficiency achievable. New high-performance materials have also meant great increases in effects and protection potential. Developments possible in the next 20 years may have similar effect on warfare as the revolution in weapons, munitions and armour that occurred in the late 19th century. The statement that ”Ballistic technology is generally considered a mature technology” is no longer true. Any nation that will abstain from following the developments closely and exploiting their advances will run the risk both of having weapons, munitions and protection that prove inadequate and of making grave mis-investments.
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5.
  • Askling, HH, et al. (author)
  • Malaria risk in travelers
  • 2005
  • In: Emerging infectious diseases. - : Centers for Disease Control and Prevention (CDC). - 1080-6040 .- 1080-6059. ; 11:3, s. 436-441
  • Journal article (peer-reviewed)
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6.
  • Askling, HH, et al. (author)
  • Travellers returning to Sweden with falciparum malaria: Pre-travel advice, behaviour, chemoprophylaxis and diagnostic delay
  • 2005
  • In: Scandinavian Journal of Infectious Diseases. - : Informa UK Limited. - 1651-1980 .- 0036-5548. ; 37:10, s. 760-765
  • Journal article (peer-reviewed)abstract
    • We have investigated pre-travel advice, behaviour, chemoprophylaxis and diagnostic delay in travellers returning to Sweden with falciparum malaria. Questionnaires were distributed to patients having been notified with falciparum malaria from 1994 to 2001. Of 408 notified patients, 237 (58%) returned the questionnaires; 62% were males and 43% above the age of 45 y. Africa was the travel destination in 90% of the cases, and 27% had travelled to Kenya. 69% had spent more than 1 night in the countryside, and 6% had stayed in modern urban areas only. 40% took an adequate dose of chemoprophylaxis, although this proportion decreased from 55% to 12% during the study period. Nine per cent used both bed nets and mosquito repellents regularly. The median time from onset of symptoms to contact with health care professionals was 2 d, and from that contact to start of malaria treatment the median time was less than 24 h.
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7.
  • Duberg, Ann-Sofi, et al. (author)
  • The epidemiology of hepatitis C virus infection in Sweden
  • 2008
  • In: Eurosurveillance. - : European Centre for Disease Prevention and Control. - 1025-496X .- 1560-7917. ; 13:21
  • Journal article (peer-reviewed)abstract
    • In Sweden, infection with hepatitis C virus (HCV) has been a notifiable disease since 1990, when diagnostic methods became available. Blood donor screening indicated that about 0.5% of the Swedish population (9 millions) had been HCV infected. Here we present the Swedish hepatitis C epidemic based on data from all the HCV notifications 1990-2006. During this time about 42,000 individuals (70% men) were diagnosed and reported as HCV infected. The majority (80%) were born in 1950 or later, with a high percentage (60%) born in the 1950s and 1960s. Younger people, 15-24 years old at notification, were reported on the same level each year. The main reported routes of HCV transmission were intravenous drug use in 65%, blood transfusions/products in 6%, and sexual in 2%, though unknown or not stated in 26%. Approximately 6,000 of all notified individuals have died during the study period. To conclude, the Swedish HCV epidemic is highly related to the increase of intravenous drug use in the late 1960s and 1970s, with a high proportion of people now chronically infected for more than 25 years, resulting in an increase of severe liver complications in form of cirrhosis and hepatocellular carcinoma. Furthermore the unchanged number of notifications of newly infected younger people indicates an ongoing HCV epidemic.PMID: 18761966 [PubMed - indexed for MEDLINE]
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9.
  • Rohrmann, Sabine, et al. (author)
  • Ethanol intake and risk of lung cancer in the European prospective investigation into cancer and nutrition (EPIC)
  • 2006
  • In: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 164:11, s. 1103-1114
  • Journal article (peer-reviewed)abstract
    • Within the European Prospective Investigation into Cancer and Nutrition (EPIC), the authors examined the association of ethanol intake at recruitment (1,119 cases) and mean lifelong ethanol intake (887 cases) with lung cancer. Information on baseline and past alcohol consumption, lifetime tobacco smoking, diet, and the anthropometric characteristics of 478,590 participants was collected between 1992 and 2000. Cox proportional hazards regression was used to calculate multivariate-adjusted hazard ratios and 95% confidence intervals. Overall, neither ethanol intake at recruitment nor mean lifelong ethanol intake was significantly associated with lung cancer. However, moderate intake (5-14.9 g/day) at recruitment (hazard ratio (HR) = 0.76, 95% confidence interval (CI): 0.63, 0.90) and moderate mean lifelong intake (HR = 0.80, 95% CI: 0.66, 0.97) were associated with a lower lung cancer risk in comparison with low consumption (0.1-4.9 g/day). Compared with low intake, a high (>= 60 g/day) mean lifelong ethanol intake tended to be related to a higher risk of lung cancer (HR = 1.29, 95% CI: 0.93, 1.74), but high intake at recruitment was not. Although there was no overall association between ethanol intake and risk of lung cancer, the authors cannot rule out a lower risk for moderate consumption and a possibly increased risk for high lifelong consumption.
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