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Träfflista för sökning "WFRF:(Vermeulen M.) srt2:(2005-2009)"

Sökning: WFRF:(Vermeulen M.) > (2005-2009)

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  • Neyens, G., et al. (författare)
  • g-Factor Measurements on Relativistic Isomeric Beams Produced by Fragmentation and U-fission: The g-RISING Project at GSI
  • 2007
  • Ingår i: Acta Physica Polonica. Series B: Elementary Particle Physics, Nuclear Physics, Statistical Physics, Theory of Relativity, Field Theory. - 0587-4254. ; 38:4, s. 1237-1247
  • Tidskriftsartikel (refereegranskat)abstract
    • Within the RISING (Rare ISotope INvestigations @ GSI) Collaboration at GSI, g factor measurements have been performed on isomeric states in neutron-rich isotopes approaching Sn-132 and in the neutron deficient Pb-region (the g-RISING campaign). We present the experimental technique and some typical aspects related to such studies on relativistic beams selected with the FRS fragment separator. First results are presented for the (19/2(+)) 4.5 mu s isomeric state in Sn-127, which has been produced by means of fission of a relativistic U-238 beam on the one hand, and by the fragmentation of a relativistic Xe-136 beam on the other hand. Spin-alignment has been observed in both reactions. It was the first time that spin-alignment has been established in a relativistic fission reaction.
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  • Lozeva, R. L., et al. (författare)
  • New sub-us Isomers in 125Sn, 127Sn, 129Sn and Isomer Systematics of 124-130Sn
  • 2008
  • Ingår i: Physical Review C (Nuclear Physics). - 0556-2813. ; 77:6
  • Tidskriftsartikel (refereegranskat)abstract
    • New sub-mu s isomers have been observed in the neutron-rich Sn isotopes. Sn-125,Sn-127,Sn-129 nuclei have been produced in a relativistic fission reaction of U-238 on a Be-9 target at 750 A.MeV and by the fragmentation of Xe-136 at 600 A.MeV populating high-spin yrast states. In addition to the already known mu s isomers, three new ones with sub-mu s half-lives have been observed. These yrast isomers are the high-spin members of the nu(d(3/2)(-1)h(11/2)(-2)) and nu h(11/2)(-n), seniority v = 3 multiplets leading to isomeric (23/2(+)) and (27/2(-)) states, respectively. Added to the already known 19/2(+)mu s isomers in this region the current work completes the systematic information of neutron-hole excitations toward the filling of the last h(11/2) orbital at N = 82. The results are discussed in the framework of state-of-the-art shell-model calculations using realistic interactions.
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  • van Es, Michael A, et al. (författare)
  • Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis
  • 2009
  • Ingår i: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 41:10, s. 1083-1087
  • Tidskriftsartikel (refereegranskat)abstract
    • We conducted a genome-wide association study among 2,323 individuals with sporadic amyotrophic lateral sclerosis (ALS) and 9,013 control subjects and evaluated all SNPs with P < 1.0 x 10(-4) in a second, independent cohort of 2,532 affected individuals and 5,940 controls. Analysis of the genome-wide data revealed genome-wide significance for one SNP, rs12608932, with P = 1.30 x 10(-9). This SNP showed robust replication in the second cohort (P = 1.86 x 10(-6)), and a combined analysis over the two stages yielded P = 2.53 x 10(-14). The rs12608932 SNP is located at 19p13.3 and maps to a haplotype block within the boundaries of UNC13A, which regulates the release of neurotransmitters such as glutamate at neuromuscular synapses. Follow-up of additional SNPs showed genome-wide significance for two further SNPs (rs2814707, with P = 7.45 x 10(-9), and rs3849942, with P = 1.01 x 10(-8)) in the combined analysis of both stages. These SNPs are located at chromosome 9p21.2, in a linkage region for familial ALS with frontotemporal dementia found previously in several large pedigrees.
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  • Friberg, L. E., et al. (författare)
  • An agonist-antagonist interaction model for prolactin release following risperidone and paliperidone treatment
  • 2009
  • Ingår i: Clinical Pharmacology and Therapeutics. - : Springer Science and Business Media LLC. - 0009-9236 .- 1532-6535. ; 85:4, s. 409-417
  • Tidskriftsartikel (refereegranskat)abstract
    • A mechanistic pharmacokinetic/pharmacodynamic model is presented, characterizing the time course of prolactin in healthy as well as schizophrenic subjects following the administration of various doses and formulations of the antipsychotic drugs risperidone and paliperidone. Prolactin concentrations from nine studies (1,462 subjects) were analyzed in NONMEM. A competitive agonist-antagonist interaction model described the competition between these drugs and dopamine for the D(2) receptors that regulate prolactin release. Tolerance development was explained by a feedback loop with prolactin stimulating dopamine release, whereas models wherein tolerance is described in terms of depletion of a prolactin pool did not explain the data well. The diurnal prolactin rhythm was described by a two-period cosine function. Baseline prolactin was health-status dependent and higher in women than in men, although the drug-induced release was less than proportional to baseline. This quantitative mechanism-based model is the first to describe prolactin release in patients, and it confirms that paliperidone and risperidone have similar potencies for prolactin release.
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  • Gallo, Valentina, et al. (författare)
  • Smoking and risk for amyotrophic lateral sclerosis : analysis of the EPIC cohort
  • 2009
  • Ingår i: Annals of Neurology. - New York : J. Wiley & Sons. - 0364-5134 .- 1531-8249. ; 65:4, s. 378-385
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrollment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2.32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure.
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