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The production of the hypertriton nuclei 3ΛH and 3Λ¯H¯¯¯¯ has been measured for the first time in Pb-Pb collisions at sNN−−−√ = 2.76 TeV with the ALICE experiment at LHC energies. The total yield, dN/dy ×B.R.(3ΛH→3He,π−)=(3.86±0.77(stat.)±0.68(syst.))×10−5 in the 0-10% most central collisions, is consistent with the predictions from a statistical thermal model using the same temperature as for the light hadrons. The coalescence parameter B3 shows a dependence on the transverse momentum, similar to the B2 of deuterons and the B3 of 3He nuclei. The ratio of yields S3 = 3ΛH/(3He ×Λ/p) was measured to be S3 = 0.60 ± 0.13 (stat.) ± 0.21 (syst.) in 0-10% centrality events; this value is compared to different theoretical models. The measured S3 is fully compatible with thermal model predictions. The measured 3ΛH lifetime, τ=181+54−39(stat.)±33(syst.) ps is compatible within 1σ with the world average value.
The production of the hypertriton nuclei 3ΛH and 3Λ¯H¯¯¯¯ has been measured for the first time in Pb-Pb collisions at sNN−−−√ = 2.76 TeV with the ALICE experiment at LHC energies. The total yield, dN/dy ×B.R.(3ΛH→3He,π−)=(3.86±0.77(stat.)±0.68(syst.))×10−5 in the 0-10% most central collisions, is consistent with the predictions from a statistical thermal model using the same temperature as for the light hadrons. The coalescence parameter B3 shows a dependence on the transverse momentum, similar to the B2 of deuterons and the B3 of 3He nuclei. The ratio of yields S3 = 3ΛH/(3He ×Λ/p) was measured to be S3 = 0.60 ± 0.13 (stat.) ± 0.21 (syst.) in 0-10% centrality events; this value is compared to different theoretical models. The measured S3 is fully compatible with thermal model predictions. The measured 3ΛH lifetime, τ=181+54−39(stat.)±33(syst.) ps is compatible within 1σ with the world average value.
The production of the hypertriton nuclei HΛ3 and H‾Λ¯3 has been measured for the first time in Pb–Pb collisions at sNN=2.76 TeV with the ALICE experiment at LHC. The pT-integrated HΛ3 yield in one unity of rapidity, dN/dy×B.R.(HΛ3→He3,π−)=(3.86±0.77(stat.)±0.68(syst.))×10−5 in the 0–10% most central collisions, is consistent with the predictions from a statistical thermal model using the same temperature as for the light hadrons. The coalescence parameter B3 shows a dependence on the transverse momentum, similar to the B2 of deuterons and the B3 of 3He nuclei. The ratio of yields S3=HΛ3/(He3×Λ/p) was measured to be S3=0.60±0.13(stat.)±0.21(syst.) in 0–10% centrality events; this value is compared to different theoretical models. The measured S3 is compatible with thermal model predictions. The measured HΛ3 lifetime, τ=181−39+54(stat.)±33(syst.)ps is in agreement within 1σ with the world average value.
Serial quantification of BCR–ABL1 mRNA is an important therapeutic indicator in chronic myeloid leukaemia, but there is a substantial variation in results reported by different laboratories. To improve comparability, an internationally accepted plasmid certified reference material (CRM) was developed according to ISO Guide 34:2009. Fragments of BCR–ABL1 (e14a2 mRNA fusion), BCR and GUSB transcripts were amplified and cloned into pUC18 to yield plasmid pIRMM0099. Six different linearised plasmid solutions were produced with the following copy number concentrations, assigned by digital PCR, and expanded uncertainties: 1.08±0.13 × 106, 1.08±0.11 × 105, 1.03±0.10 × 104, 1.02±0.09 × 103, 1.04±0.10 × 102 and 10.0±1.5 copies/μl. The certification of the material for the number of specific DNA fragments per plasmid, copy number concentration of the plasmid solutions and the assessment of inter-unit heterogeneity and stability were performed according to ISO Guide 35:2006. Two suitability studies performed by 63 BCR–ABL1 testing laboratories demonstrated that this set of 6 plasmid CRMs can help to standardise a number of measured transcripts of e14a2 BCR–ABL1 and three control genes (ABL1, BCR and GUSB). The set of six plasmid CRMs is distributed worldwide by the Institute for Reference Materials and Measurements (Belgium) and its authorised distributors (https://ec.europa.eu/jrc/en/reference-materials/catalogue/; CRM code ERM-AD623a-f).
Although autism spectrum disorders (ASDs) have a substantial genetic basis, most of the known genetic risk has been traced to rare variants, principally copy number variants (CNVs). To identify common risk variation, the Autism Genome Project (AGP) Consortium genotyped 1558 rigorously defined ASD families for 1 million single-nucleotide polymorphisms (SNPs) and analyzed these SNP genotypes for association with ASD. In one of four primary association analyses, the association signal for marker rs4141463, located within MACROD2, crossed the genome-wide association significance threshold of P < 5 × 10−8. When a smaller replication sample was analyzed, the risk allele at rs4141463 was again over-transmitted; yet, consistent with the winner's curse, its effect size in the replication sample was much smaller; and, for the combined samples, the association signal barely fell below the P < 5 × 10−8 threshold. Exploratory analyses of phenotypic subtypes yielded no significant associations after correction for multiple testing. They did, however, yield strong signals within several genes, KIAA0564, PLD5, POU6F2, ST8SIA2 and TAF1C.
Autism spectrum disorder (ASD) is a highly heritable disorder of complex and heterogeneous aetiology. It is primarily characterized by altered cognitive ability including impaired language and communication skills and fundamental deficits in social reciprocity. Despite some notable successes in neuropsychiatric genetics, overall, the high heritability of ASD (~90%) remains poorly explained by common genetic risk variants. However, recent studies suggest that rare genomic variation, in particular copy number variation, may account for a significant proportion of the genetic basis of ASD. We present a large scale analysis to identify candidate genes which may contain low-frequency recessive variation contributing to ASD while taking into account the potential contribution of population differences to the genetic heterogeneity of ASD. Our strategy, homozygous haplotype (HH) mapping, aims to detect homozygous segments of identical haplotype structure that are shared at a higher frequency amongst ASD patients compared to parental controls. The analysis was performed on 1,402 Autism Genome Project trios genotyped for 1 million single nucleotide polymorphisms (SNPs). We identified 25 known and 1,218 novel ASD candidate genes in the discovery analysis including CADM2, ABHD14A, CHRFAM7A, GRIK2, GRM3, EPHA3, FGF10, KCND2, PDZK1, IMMP2L and FOXP2. Furthermore, 10 of the previously reported ASD genes and 300 of the novel candidates identified in the discovery analysis were replicated in an independent sample of 1,182 trios. Our results demonstrate that regions of HH are significantly enriched for previously reported ASD candidate genes and the observed association is independent of gene size (odds ratio 2.10). Our findings highlight the applicability of HH mapping in complex disorders such as ASD and offer an alternative approach to the analysis of genome-wide association data.
Background: Intracerebral haemorrhage growth is associated with poor clinical outcome and is a therapeutic target for improving outcome. We aimed to determine the absolute risk and predictors of intracerebral haemorrhage growth, develop and validate prediction models, and evaluate the added value of CT angiography.
Methods: In a systematic review of OVID MEDLINE—with additional hand-searching of relevant studies' bibliographies— from Jan 1, 1970, to Dec 31, 2015, we identified observational cohorts and randomised trials with repeat scanning protocols that included at least ten patients with acute intracerebral haemorrhage. We sought individual patient-level data from corresponding authors for patients aged 18 years or older with data available from brain imaging initially done 0·5–24 h and repeated fewer than 6 days after symptom onset, who had baseline intracerebral haemorrhage volume of less than 150 mL, and did not undergo acute treatment that might reduce intracerebral haemorrhage volume. We estimated the absolute risk and predictors of the primary outcome of intracerebral haemorrhage growth (defined as >6 mL increase in intracerebral haemorrhage volume on repeat imaging) using multivariable logistic regression models in development and validation cohorts in four subgroups of patients, using a hierarchical approach: patients not taking anticoagulant therapy at intracerebral haemorrhage onset (who constituted the largest subgroup), patients taking anticoagulant therapy at intracerebral haemorrhage onset, patients from cohorts that included at least some patients taking anticoagulant therapy at intracerebral haemorrhage onset, and patients for whom both information about anticoagulant therapy at intracerebral haemorrhage onset and spot sign on acute CT angiography were known.
Findings: Of 4191 studies identified, 77 were eligible for inclusion. Overall, 36 (47%) cohorts provided data on 5435 eligible patients. 5076 of these patients were not taking anticoagulant therapy at symptom onset (median age 67 years, IQR 56–76), of whom 1009 (20%) had intracerebral haemorrhage growth. Multivariable models of patients with data on antiplatelet therapy use, data on anticoagulant therapy use, and assessment of CT angiography spot sign at symptom onset showed that time from symptom onset to baseline imaging (odds ratio 0·50, 95% CI 0·36–0·70; p<0·0001), intracerebral haemorrhage volume on baseline imaging (7·18, 4·46–11·60; p<0·0001), antiplatelet use (1·68, 1·06–2·66; p=0·026), and anticoagulant use (3·48, 1·96–6·16; p<0·0001) were independent predictors of intracerebral haemorrhage growth (C-index 0·78, 95% CI 0·75–0·82). Addition of CT angiography spot sign (odds ratio 4·46, 95% CI 2·95–6·75; p<0·0001) to the model increased the C-index by 0·05 (95% CI 0·03–0·07).
Interpretation: In this large patient-level meta-analysis, models using four or five predictors had acceptable to good discrimination. These models could inform the location and frequency of observations on patients in clinical practice, explain treatment effects in prior randomised trials, and guide the design of future trials.
Funding: UK Medical Research Council and British Heart Foundation.
The interaction between Λ baryons and kaons/antikaons is a crucial ingredient for the strangeness S=0 and S=−2 sector of the meson--baryon interaction at low energies. In particular, the ΛK¯¯¯¯ might help in understanding the origin of states such as the Ξ(1620), whose nature and properties are still under debate. Experimental data on Λ−K and Λ−K¯¯¯¯ systems are scarce, leading to large uncertainties and tension between the available theoretical predictions constrained by such data. In this Letter we present the measurements of Λ−K+⊕Λ¯¯¯¯−K− and Λ−K−⊕Λ¯¯¯¯−K+ correlations obtained in the high-multiplicity triggered data sample in pp collisions at s√=13 TeV recorded by ALICE at the LHC. The correlation function for both pairs is modeled using the Lednicky−Lyuboshits analytical formula and the corresponding scattering parameters are extracted. The Λ−K−⊕Λ¯¯¯¯−K+ correlations show the presence of several structures at relative momenta k∗ above 200 MeV/c, compatible with the Ω baryon, the Ξ(1690), and Ξ(1820) resonances decaying into Λ−K− pairs. The low k∗ region in the Λ−K−⊕Λ¯¯¯¯−K+ also exhibits the presence of the Ξ(1620) state, expected to strongly couple to the measured pair. The presented data allow to access the ΛK+ and ΛK− strong interaction with an unprecedented precision and deliver the first experimental observation of the Ξ(1620) decaying into ΛK−.
The interaction between Λ baryons and kaons/antikaons is a crucial ingredient for the strangeness S=0 and S=−2 sector of the meson–baryon interaction at low energies. In particular, the ΛK‾ might help in understanding the origin of states such as the Ξ(1620), whose nature and properties are still under debate. Experimental data on Λ–K and Λ–K‾ systems are scarce, leading to large uncertainties and tension between the available theoretical predictions constrained by such data. In this Letter we present the measurements of Λ–K⊕+Λ‾–K− and Λ–K⊕−Λ‾–K+ correlations obtained in the high-multiplicity triggered data sample in pp collisions at s=13 TeV recorded by ALICE at the LHC. The correlation function for both pairs is modeled using the Lednický–Lyuboshits analytical formula and the corresponding scattering parameters are extracted. The Λ–K⊕−Λ‾–K+ correlations show the presence of several structures at relative momenta k⁎ above 200 MeV/c, compatible with the Ω baryon, the Ξ(1690), and Ξ(1820) resonances decaying into Λ–K− pairs. The low k⁎ region in the Λ–K⊕−Λ‾–K+ also exhibits the presence of the Ξ(1620) state, expected to strongly couple to the measured pair. The presented data allow to access the ΛK+ and ΛK− strong interaction with an unprecedented precision and deliver the first experimental observation of the Ξ(1620) decaying into ΛK−.
The interaction between Λ baryons and kaons/antikaons is a crucial ingredient for the strangeness S=0 and S=−2 sector of the meson--baryon interaction at low energies. In particular, the ΛK¯¯¯¯ might help in understanding the origin of states such as the Ξ(1620), whose nature and properties are still under debate. Experimental data on Λ−K and Λ−K¯¯¯¯ systems are scarce, leading to large uncertainties and tension between the available theoretical predictions constrained by such data. In this Letter we present the measurements of Λ−K+⊕Λ¯¯¯¯−K− and Λ−K−⊕Λ¯¯¯¯−K+ correlations obtained in the high-multiplicity triggered data sample in pp collisions at s√=13 TeV recorded by ALICE at the LHC. The correlation function for both pairs is modeled using the Lednicky−Lyuboshits analytical formula and the corresponding scattering parameters are extracted. The Λ−K−⊕Λ¯¯¯¯−K+ correlations show the presence of several structures at relative momenta k∗ above 200 MeV/c, compatible with the Ω baryon, the Ξ(1690), and Ξ(1820) resonances decaying into Λ−K− pairs. The low k∗ region in the Λ−K−⊕Λ¯¯¯¯−K+ also exhibits the presence of the Ξ(1620) state, expected to strongly couple to the measured pair. The presented data allow to access the ΛK+ and ΛK− strong interaction with an unprecedented precision and deliver the first experimental observation of the Ξ(1620) decaying into ΛK−.