13 research outputs found
Particularized protection: UNSC mandates and the protection of civilians in armed conflict
The protection of civilians at risk in armed conflict has, since the late 1990s, become institutionalized at the United Nations (UN), gaining acceptance as a normative rationale for UN peacekeeping. However, the bulk of civilians in need of protection in armed conflict are unlikely to attain it. The article develops an argument on ‘particularized protection’ - particularized in that UN Security Council (SC) mandates are formulated and adjusted over time to direct mission protection to specific subsets of civilian populations, that is, those relevant to the UN itself, the host state, other states, NGOs and the media, leaving most local civilians receiving little effective protection. Particularized protection, we argue, is a result of the institutional dynamics involving actors producing mandates - the UNSC - and those providing protection - peacekeeping missions - whereby mandates are specified to direct mission protection to selected, particularized groups. We demonstrate these dynamics in two cases, Côte d’Ivoire and Somalia
A selection of Slovenian literary heroes for the preschool period
V vrtcih slovenske literarne junake vse bolj spodrivajo tuji fantazijski junaki, za katere se otroci navdušijo prek risank, revij in video igric. Slovenski junaki so pomemben del naše kulture in so lahko nekakšni spremljevalci v domovinski vzgoji pri najmlajših. To delo naj služi kot promocija slovenskih literarnih junakov pri otrocih vseh starosti, z začetkom v predšolskem obdobju. V delu je opredeljeno merilo izbire likovpredstavljene so njihove zgodbe, posebne lastnosti in upodobitevjunaki so po izvoru opredeljeni kot ljudski ali umetninavedeni so avtorji in zgodovinske okoliščine nastankaraziskane so njihova prepoznavnost in zastopanost v različnih medijih (slikanice, avdio- in video mediji, oglasi) ter dostopnost teh medijev.In preschools, Slovenian literary heroes are being displaced by foreign fantastic heroes that impress children via cartoons, magazines and video games. Slovenian heroes are an important part of our culture and can act as companions of sorts within citizenship education of youngsters. This thesis should serve as a promotion of Slovenian literary heroes for children of all ages, beginning with the preschool period. The thesis defines the selection criterion of charactersit introduces their stories, special characteristics and depictionsit defines heroes by origin as folk or artificialit lists the authors and historical circumstances of productionit investigates their recognisability and representation in various media (picture books, audio- and video media, advertisements) and the accessibility of these media
Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33
Genome-wide association studies (GWAS) have mapped risk alleles for at
least 10 distinct cancers to a small region of 63 000 bp on chromosome
5p15.33. This region harbors the TERT and CLPTM1L genes; the former
encodes the catalytic subunit of telomerase reverse transcriptase and
the latter may play a role in apoptosis. To investigate further the
genetic architecture of common susceptibility alleles in this region, we
conducted an agnostic subset-based meta-analysis (association analysis
based on subsets) across six distinct cancers in 34 248 cases and 45 036
controls. Based on sequential conditional analysis, we identified as
many as six independent risk loci marked by common single-nucleotide
polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 x
10(-39); Region 3: rs2853677, P = 3.30 x 10(-36) and P-Conditional =
2.36 x 10(-8); Region 4: rs2736098, P = 3.87 x 10(-12) and P-Conditional
= 5.19 x 10(-6), Region 5: rs13172201, P = 0.041 and P-Conditional =
2.04 x 10(-6); and Region 6: rs10069690, P = 7.49 x 10 215 and
P-Conditional = 5.35 x 10(-7)) and one in the neighboring CLPTM1L
gene(Region 2: rs451360; P = 1.90 x 10(-18) and P-Conditional = 7.06 x
10(-16)). Between three and five cancers mapped to each independent
locus with both risk-enhancing and protective effects. Allele-specific
effects on DNA methylation were seen for a subset of risk loci,
indicating that methylation and subsequent effects on gene expression
may contribute to the biology of risk variants on 5p15.33. Our results
provide strong support for extensive pleiotropy across this region of
5p15.33, to an extent not previously observed in other cancer
susceptibility loci
Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for Thirteen Cancer Types
BACKGROUND: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. METHODS: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. RESULTS: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. CONCLUSION: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation
Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for Thirteen Cancer Types
BACKGROUND: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. METHODS: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. RESULTS: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. CONCLUSION: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation
Analysis of heritability and shared heritability based on genome-wide association studies for 13 cancer types
Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl², on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.11 page(s
Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
Background: Studies of related individuals have consistently
demonstrated notable familial aggregation of cancer. We aim to estimate
the heritability and genetic correlation attributable to the additive
effects of common single-nucleotide polymorphisms (SNPs) for cancer at
13 anatomical sites.
Methods: Between 2007 and 2014, the US National Cancer Institute has
generated data from genome-wide association studies (GWAS) for 49 492
cancer case patients and 34 131 control patients. We apply novel mixed
model methodology (GCTA) to this GWAS data to estimate the heritability
of individual cancers, as well as the proportion of heritability
attributable to cigarette smoking in smoking-related cancers, and the
genetic correlation between pairs of cancers.
Results: GWAS heritability was statistically significant at nearly all
sites, with the estimates of array-based heritability, h(l)(2), on the
liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the
combined heritability of multiple smoking characteristics, we calculate
that at least 24% (95% confidence interval [CI] = 14% to 37%) and
7% (95% CI = 4% to 11%) of the heritability for lung and bladder
cancer, respectively, can be attributed to genetic determinants of
smoking. Most pairs of cancers studied did not show evidence of strong
genetic correlation. We found only four pairs of cancers with marginally
statistically significant correlations, specifically kidney and testes
(rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and
pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic
lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung
(rho = 0.35, SE = 0.14). Correlation analysis also indicates that the
genetic architecture of lung cancer differs between a smoking population
of European ancestry and a nonsmoking Asian population, allowing for the
possibility that the genetic etiology for the same disease can vary by
population and environmental exposures.
Conclusion: Our results provide important insights into the genetic
architecture of cancers and suggest new avenues for investigation