155 research outputs found

    Transition from elastic to plastic strain release in core−shell nanowires revealed by in-plane x-ray diffraction

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    We investigate the strain evolution and relaxation process as function of increasing lattice mismatch between the GaAs core and surrounding InxGa1x_{1-x}As shell in core–shell nanowire heterostructures grown on Si(111) substrates. The dimensions of the core and shell are kept constant whereas the indium concentration inside the shell is varied. Measuring the 224ˉ22\bar{4} and 22ˉ02\bar{2}0 in-plane Bragg reflections normal to the nanowire side edges and side facets, we observe a transition from elastic to plastic strain release for a shell indium content x > 0.5. Above the onset of plastic strain relaxation, indium rich mounds and an indium poor coherent shell grow simultaneously around the GaAs core. Mound formation was observed for indium contents x = 0.5 and 0.6 by scanning electron microscopy. Considering both the measured radial reflections and the axial 111 Bragg reflection, the 3D strain variation was extracted separately for the core and the InxGa1x_{1-x}As shell

    Measurement of the CKM Matrix Element Vcb|V_{cb}| from B0D+νB^{0} \to D^{*-} \ell^+ \nu_\ell at Belle

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    We present a new measurement of the CKM matrix element Vcb|V_{cb}| from B0D+νB^{0} \to D^{*-} \ell^+ \nu_\ell decays, reconstructed with the full Belle data set of 711fb1711 \, \rm fb^{-1} integrated luminosity. Two form factor parameterizations, originally conceived by the Caprini-Lellouch-Neubert (CLN) and the Boyd, Grinstein and Lebed (BGL) groups, are used to extract the product F(1)ηEWVcb\mathcal{F}(1)\eta_{\rm EW}|V_{cb}| and the decay form factors, where F(1)\mathcal{F}(1) is the normalization factor and ηEW\eta_{\rm EW} is a small electroweak correction. In the CLN parameterization we find F(1)ηEWVcb=(35.06±0.15±0.56)×103\mathcal{F}(1)\eta_{\rm EW}|V_{cb}| = (35.06 \pm 0.15 \pm 0.56) \times 10^{-3}, ρ2=1.106±0.031±0.007\rho^{2}=1.106 \pm 0.031 \pm 0.007, R1(1)=1.229±0.028±0.009R_{1}(1)=1.229 \pm 0.028 \pm 0.009, R2(1)=0.852±0.021±0.006R_{2}(1)=0.852 \pm 0.021 \pm 0.006. For the BGL parameterization we obtain F(1)ηEWVcb=(34.93±0.23±0.59)×103\mathcal{F}(1)\eta_{\rm EW}|V_{cb}|= (34.93 \pm 0.23 \pm 0.59)\times 10^{-3}, which is consistent with the World Average when correcting for F(1)ηEW\mathcal{F}(1)\eta_{\rm EW}. The branching fraction of B0D+νB^{0} \to D^{*-} \ell^+ \nu_\ell is measured to be B(B0D+ν)=(4.90±0.02±0.16)%\mathcal{B}(B^{0}\rightarrow D^{*-}\ell^{+}\nu_{\ell}) = (4.90 \pm 0.02 \pm 0.16)\%. We also present a new test of lepton flavor universality violation in semileptonic BB decays, B(B0De+ν)B(B0Dμ+ν)=1.01±0.01±0.03 \frac{{\cal B }(B^0 \to D^{*-} e^+ \nu)}{{\cal B }(B^0 \to D^{*-} \mu^+ \nu)} = 1.01 \pm 0.01 \pm 0.03~. The errors correspond to the statistical and systematic uncertainties respectively. This is the most precise measurement of F(1)ηEWVcb\mathcal{F}(1)\eta_{\rm EW}|V_{cb}| and form factors to date and the first experimental study of the BGL form factor parameterization in an experimental measurement

    Search for CPCP violation in the D+π+π0D^{+}\to\pi^{+}\pi^{0} decay at Belle

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    We search for CPCP violation in the charged charm meson decay D+π+π0D^{+}\to\pi^{+}\pi^{0}, based on a data sample corresponding to an integrated luminosity of 921 fb1\rm 921~fb^{-1} collected by the Belle experiment at the KEKB e+ee^{+}e^{-} asymmetric-energy collider. The measured CPCP violating asymmetry is [+2.31±1.24(stat)±0.23(syst)]%[+2.31\pm1.24({\rm stat})\pm0.23({\rm syst})]\%, which is consistent with the standard model prediction and has a significantly improved precision compared to previous results.Comment: 8 pages, 3 figure

    Measurement of the branching fraction and CPCP asymmetry in B0π0π0B^{0} \to \pi^{0}\pi^{0} decays, and an improved constraint on ϕ2\phi_{2}

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    We measure the branching fraction and CPCP violation asymmetry in the decay B0π0π0B^{0}\to \pi^{0}\pi^{0}, using a data sample of 752×106752\times 10^{6} BBˉB\bar{B} pairs collected at the Υ(4S)\Upsilon(4S) resonance with the Belle detector at the KEKB e+ee^{+}e^{-} collider. The obtained branching fraction and direct CPCP asymmetry are B(Bπ0π0)=[1.31±0.19 (stat.)±0.19 (syst.)]×106 \mathcal{B}(B\to \pi^{0}\pi^{0}) = [1.31 \pm 0.19~ \text{(stat.)} \pm 0.19~ \text{(syst.)}] \times 10^{-6} and ACP=+0.14±0.36 (stat.)±0.10 (syst.), A_{CP} = +0.14 \pm 0.36~ \text{(stat.)} \pm 0.10~ \text{(syst.)}, respectively. The signal significance, including the systematic uncertainty, is 6.4 standard deviations. We combine these results with Belle's earlier measurements of B0π+πB^{0}\to \pi^{+} \pi^{-} and B±π±π0B^{\pm} \to \pi^{\pm} \pi^{0} to exclude the CPCP-violating parameter ϕ2\phi_{2} from the range 15.5<ϕ2<75.015.5^{\circ} < \phi_{2} < 75.0^{\circ} at 95\% confidence level.Comment: 8 pages, 2 figure

    The global burden of adolescent and young adult cancer in 2019: a systematic analysis for the Global Burden of Disease Study 2019

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    Background: In estimating the global burden of cancer, adolescents and young adults with cancer are often overlooked, despite being a distinct subgroup with unique epidemiology, clinical care needs, and societal impact. Comprehensive estimates of the global cancer burden in adolescents and young adults (aged 15–39 years) are lacking. To address this gap, we analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, with a focus on the outcome of disability-adjusted life-years (DALYs), to inform global cancer control measures in adolescents and young adults. Methods: Using the GBD 2019 methodology, international mortality data were collected from vital registration systems, verbal autopsies, and population-based cancer registry inputs modelled with mortality-to-incidence ratios (MIRs). Incidence was computed with mortality estimates and corresponding MIRs. Prevalence estimates were calculated using modelled survival and multiplied by disability weights to obtain years lived with disability (YLDs). Years of life lost (YLLs) were calculated as age-specific cancer deaths multiplied by the standard life expectancy at the age of death. The main outcome was DALYs (the sum of YLLs and YLDs). Estimates were presented globally and by Socio-demographic Index (SDI) quintiles (countries ranked and divided into five equal SDI groups), and all estimates were presented with corresponding 95% uncertainty intervals (UIs). For this analysis, we used the age range of 15–39 years to define adolescents and young adults. Findings: There were 1·19 million (95% UI 1·11–1·28) incident cancer cases and 396 000 (370 000–425 000) deaths due to cancer among people aged 15–39 years worldwide in 2019. The highest age-standardised incidence rates occurred in high SDI (59·6 [54·5–65·7] per 100 000 person-years) and high-middle SDI countries (53·2 [48·8–57·9] per 100 000 person-years), while the highest age-standardised mortality rates were in low-middle SDI (14·2 [12·9–15·6] per 100 000 person-years) and middle SDI (13·6 [12·6–14·8] per 100 000 person-years) countries. In 2019, adolescent and young adult cancers contributed 23·5 million (21·9–25·2) DALYs to the global burden of disease, of which 2·7% (1·9–3·6) came from YLDs and 97·3% (96·4–98·1) from YLLs. Cancer was the fourth leading cause of death and tenth leading cause of DALYs in adolescents and young adults globally. Interpretation: Adolescent and young adult cancers contributed substantially to the overall adolescent and young adult disease burden globally in 2019. These results provide new insights into the distribution and magnitude of the adolescent and young adult cancer burden around the world. With notable differences observed across SDI settings, these estimates can inform global and country-level cancer control efforts. Funding: Bill &amp; Melinda Gates Foundation, American Lebanese Syrian Associated Charities, St Baldrick's Foundation, and the National Cancer Institute

    Measurements of branching fraction and direct CP asymmetry in B±^{±} → K0^{0}S_{S}K0^{0}S_{S}K±^{±} and a search for B±^{±} → K0^{0}S_{S}K0^{0}S_{S}π±^{±}

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    Search for the lepton-flavor-violating decay B⁰ → K0^{*0} μ±^{\pm} e^{\mp}

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    Search for B0^{0} -> X(3872)gamma

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    Mapping geographical inequalities in childhood diarrhoeal morbidity and mortality in low-income and middle-income countries, 2000–17 : analysis for the Global Burden of Disease Study 2017

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    Background Across low-income and middle-income countries (LMICs), one in ten deaths in children younger than 5 years is attributable to diarrhoea. The substantial between-country variation in both diarrhoea incidence and mortality is attributable to interventions that protect children, prevent infection, and treat disease. Identifying subnational regions with the highest burden and mapping associated risk factors can aid in reducing preventable childhood diarrhoea. Methods We used Bayesian model-based geostatistics and a geolocated dataset comprising 15 072 746 children younger than 5 years from 466 surveys in 94 LMICs, in combination with findings of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017, to estimate posterior distributions of diarrhoea prevalence, incidence, and mortality from 2000 to 2017. From these data, we estimated the burden of diarrhoea at varying subnational levels (termed units) by spatially aggregating draws, and we investigated the drivers of subnational patterns by creating aggregated risk factor estimates. Findings The greatest declines in diarrhoeal mortality were seen in south and southeast Asia and South America, where 54·0% (95% uncertainty interval [UI] 38·1–65·8), 17·4% (7·7–28·4), and 59·5% (34·2–86·9) of units, respectively, recorded decreases in deaths from diarrhoea greater than 10%. Although children in much of Africa remain at high risk of death due to diarrhoea, regions with the most deaths were outside Africa, with the highest mortality units located in Pakistan. Indonesia showed the greatest within-country geographical inequality; some regions had mortality rates nearly four times the average country rate. Reductions in mortality were correlated to improvements in water, sanitation, and hygiene (WASH) or reductions in child growth failure (CGF). Similarly, most high-risk areas had poor WASH, high CGF, or low oral rehydration therapy coverage. Interpretation By co-analysing geospatial trends in diarrhoeal burden and its key risk factors, we could assess candidate drivers of subnational death reduction. Further, by doing a counterfactual analysis of the remaining disease burden using key risk factors, we identified potential intervention strategies for vulnerable populations. In view of the demands for limited resources in LMICs, accurately quantifying the burden of diarrhoea and its drivers is important for precision public health
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