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Concepts for detritiation of waste liquids
Tritium is formed in thermal nuclear reactors both by neutron activation of elements such as deuterium and lithium and by ternary fission in the fuel. It is a weak beta-emitter with a short half-life, 12.3 years, and its radiological significance in reactor discharges is very low. In heavy-water-cooled and -moderated reactors, such as the SRS reactors, the tritium concentration in the moderator is sufficiently high to cause a potential hazard to operators, so research and development programs have been carried out on processes to remove the tritium. Detritiation of light water has also been the subject of major R D efforts world-wide, because reprocessing operations can generate significant quantities of tritium in liquid waste, and high concentrations of tritium may arise in some aqueous streams in future fusion reactors. This paper presents a review of some of the methods that have been proposed, studied, and developed for removal of tritium from light and heavy water, along with some new concepts for aqueous detritiation directly from liquid oxide (HTO) bearing feed streams
The -dependence of the generalised Gerasimov-Drell-Hearn integral for the deuteron, proton and neutron
The Gerasimov-Drell-Hearn (GDH) sum rule connects the anomalous contribution
to the magnetic moment of the target nucleus with an energy-weighted integral
of the difference of the helicity-dependent photoabsorption cross sections. The
data collected by HERMES with a deuterium target are presented together with a
re-analysis of previous measurements on the proton. This provides a measurement
of the generalised GDH integral covering simultaneously the nucleon-resonance
and the deep inelastic scattering regions. The contribution of the
nucleon-resonance region is seen to decrease rapidly with increasing . The
DIS contribution is sizeable over the full measured range, even down to the
lowest measured . As expected, at higher the data are found to be in
agreement with previous measurements of the first moment of . From data on
the deuteron and proton, the GDH integral for the neutron has been derived and
the proton--neutron difference evaluated. This difference is found to satisfy
the fundamental Bjorken sum rule at GeV.Comment: 12 pages, 10 figure
Observation of a Coherence Length Effect in Exclusive Rho^0 Electroproduction
Exclusive incoherent electroproduction of the rho^0(770) meson from 1H, 2H,
3He, and 14N targets has been studied by the HERMES experiment at squared
four-momentum transfer Q**2>0.4 GeV**2 and positron energy loss nu from 9 to 20
GeV. The ratio of the 14N to 1H cross sections per nucleon, known as the
nuclear transparency, was found to decrease with increasing coherence length of
quark-antiquark fluctuations of the virtual photon. The data provide clear
evidence of the interaction of the quark- antiquark fluctuations with the
nuclear medium.Comment: RevTeX, 5 pages, 3 figure
Determination of the Deep Inelastic Contribution to the Generalised Gerasimov-Drell-Hearn Integral for the Proton and Neutron
The virtual photon absorption cross section differences [sigma_1/2-sigma_3/2]
for the proton and neutron have been determined from measurements of polarised
cross section asymmetries in deep inelastic scattering of 27.5 GeV
longitudinally polarised positrons from polarised 1H and 3He internal gas
targets. The data were collected in the region above the nucleon resonances in
the kinematic range nu < 23.5 GeV and 0.8 GeV**2 < Q**2 < 12 GeV**2. For the
proton the contribution to the generalised Gerasimov-Drell-Hearn integral was
found to be substantial and must be included for an accurate determination of
the full integral. Furthermore the data are consistent with a QCD
next-to-leading order fit based on previous deep inelastic scattering data.
Therefore higher twist effects do not appear significant.Comment: 6 pages, 3 figures, 1 table, revte
Mendelian randomisation study of height and body mass index as modifiers of ovarian cancer risk in 22,588 BRCA1 and BRCA2 mutation carriers
Item does not contain fulltextBACKGROUND: Height and body mass index (BMI) are associated with higher ovarian cancer risk in the general population, but whether such associations exist among BRCA1/2 mutation carriers is unknown. METHODS: We applied a Mendelian randomisation approach to examine height/BMI with ovarian cancer risk using the Consortium of Investigators for the Modifiers of BRCA1/2 (CIMBA) data set, comprising 14,676 BRCA1 and 7912 BRCA2 mutation carriers, with 2923 ovarian cancer cases. We created a height genetic score (height-GS) using 586 height-associated variants and a BMI genetic score (BMI-GS) using 93 BMI-associated variants. Associations were assessed using weighted Cox models. RESULTS: Observed height was not associated with ovarian cancer risk (hazard ratio [HR]: 1.07 per 10-cm increase in height, 95% confidence interval [CI]: 0.94-1.23). Height-GS showed similar results (HR = 1.02, 95% CI: 0.85-1.23). Higher BMI was significantly associated with increased risk in premenopausal women with HR = 1.25 (95% CI: 1.06-1.48) and HR = 1.59 (95% CI: 1.08-2.33) per 5-kg/m(2) increase in observed and genetically determined BMI, respectively. No association was found for postmenopausal women. Interaction between menopausal status and BMI was significant (Pinteraction < 0.05). CONCLUSION: Our observation of a positive association between BMI and ovarian cancer risk in premenopausal BRCA1/2 mutation carriers is consistent with findings in the general population
Associations of common breast cancer susceptibility alleles with risk of breast cancer subtypes in BRCA1 and BRCA2 mutation carriers
Introduction: More than 70 common alleles are known to be involved in breast cancer (BC) susceptibility, and several exhibit significant heterogeneity in their associations with different BC subtypes. Although there are differences in the association patterns between BRCA1 and BRCA2 mutation carriers and the general population for several loci, no study has comprehensively evaluated the associations of all known BC susceptibility alleles with risk of BC subtypes in BRCA1 and BRCA2 carriers. Methods: We used data from 15,252 BRCA1 and 8,211 BRCA2 carriers to analyze the associations between approximately 200,000 genetic variants on the iCOGS array and risk of BC subtypes defined by estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and triple-negative- (TN) status; morphologic subtypes; histological grade; and nodal involvement. Results: The estimated BC hazard ratios (HRs) for the 74 known BC alleles in BRCA1 carriers exhibited moderate correlations with the corresponding odds ratios from the general population. However, their associations with ER-positive BC in BRCA1 carriers were more consistent with the ER-positive as
Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus
A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3′-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk
Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk
BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7×10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4×10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4×10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat
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