| 1. |
- Ablikim, M., et al.
(författare)
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First measurement of e(+)e(-) -> pK(S)(0)(n)over-barK(-) + c.c. above open charm threshold
- 2018
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Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 98:3
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Tidskriftsartikel (refereegranskat)abstract
- The process e(+)e(-) -> pK(S)(0)(n) over barK(-) + c.c. and its intermediate processes are studied for the first time, using data samples collected with the BESIII detector at BEPCII at center-of-mass energies of 3.773, 4.008, 4.226, 4.258, 4.358, 4.416, and 4.600 GeV, with a total integrated luminosity of 7.4 fb(-1). The Born cross section of e(+)e(-) -> pK(S)(0)(n) over barK(-) + c.c. is measured at each center-of-mass energy, but no significant resonant structure in the measured cross-section line shape between 3.773 and 4.600 GeV is observed. No evident structure is detected in the pK(-), nK(S)(0), pK(S)(0), nK(+), p (n) over bar, or (KSK-)-K-0 invariant mass distributions except for Lambda(1520). The Born cross sections of e(+)e(-) -> Lambda(1520)(n) over barK(S)(0) + c.c. and e(+)e(-) -> Lambda(1520)(p) over barK(+) + c.c. are measured, and the 90% confidence level upper limits on the Born cross sections of e(+)e(-) -> Lambda(1520)(Lambda) over bar (1520) are determined at the seven center-of-mass energies. There is an evident difference in line shape and magnitude of the measured cross sections between e(+)e(-) -> Lambda(1520)(-> pK(-))(n) over barK(S)(0) and e(+)e(-) -> pK-(Lambda) over bar (1520)(-> (n) over barK(S)(0)).
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| 2. |
- Ablikim, M., et al.
(författare)
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Observation of the Semileptonic Decay D-0 -> a(0)(980)(-)e(+)nu(e) and Evidence for D+ -> a(0)(980)(0)e(+)nu(e)
- 2018
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Ingår i: Physical Review Letters. - : AMER PHYSICAL SOC. - 0031-9007 .- 1079-7114. ; 121:8
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Tidskriftsartikel (refereegranskat)abstract
- Using an e(+)e(-) collision data sample of 2.93 fb(-1) collected at a center-of-mass energy of 3.773 GeV by the BESIII detector at BEPCII, we report the observation of D-0 -> a(0)(980)(-)e(+)nu(e) and evidence for D+ -> a(0)(980)(0)e(+)nu(e) with significances of 6.4 sigma and 2.9 sigma, respectively. The absolute branching fractions are determined to be B(D-0 -> a(0)(980)(-)e(+)nu(e)) x B(a(0)(980)(-) -> eta pi(-)) = [1.33(-0.29)(+0.33)(stat) +/- 0.09(syst)] x 10(-4) and B(D+ -> a(0)(980)(0)e(+)nu(e)) x B(a(0)(980)(0) -> eta pi(0)) = [1.66(-0.66)(+0.81)(stat) +/- 0.11(syst) x 10(-4). This is the first time the a(0)(980) meson has been measured in a D-0 semileptonic decay, which would open one more interesting page in the investigation of the nature of the puzzling a(0)(980) states.
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| 3. |
- Ablikim, M., et al.
(författare)
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Search for invisible decays of omega and phi with J/psi data at BESIII
- 2018
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Ingår i: Physical Review D. - : American Physical Society. - 2470-0010 .- 2470-0029. ; 98:3
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Tidskriftsartikel (refereegranskat)abstract
- Using a data sample of (1310.6 +/- 7.0) x 10(6) J/psi events collected with the BESIII detector operating at the BEPCII collider, we perform the first experimental search for invisible decays of a light vector meson (V = omega, phi) via J/psi -> V-eta decays. The decay of eta -> pi(+)pi(-)pi(0) is utilized to tag the V meson decaying into the invisible final state. No evidence for a significant invisible signal is observed, and the upper limits on the ratio of branching fractions at the 90% confidence level are determined to be B(omega -> invisible)/B(omega -> pi(+)pi(-)pi(0)) < 8.1 x 10(-5) and B(phi -> invisible)/B(phi -> K+K-) < 3.4 x 10(-4). By using the world average values of B(omega -> pi(+)pi(-)pi(0) and B(phi -> K+K-,) the upper limits on the decay branching fractions at the 90% confidence level are set as B(omega -> invisible) < 7.3 x 10(-5) and B(phi -> invisible) < 1.7 x 10(-4), respectively.
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| 4. |
- Ablikim, M., et al.
(författare)
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Search for the rare decays D -> h(h((')))e(+) e(-)
- 2018
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Ingår i: Physical Review D. - : AMER PHYSICAL SOC. - 2470-0010 .- 2470-0029. ; 97:7
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Tidskriftsartikel (refereegranskat)abstract
- We search for rare decays of D mesons to hadrons accompanied by an electron-positron pair (h(h((')))e(+)e(- )),using an e(+)e(-) collision sample corresponding to an integrated luminosity of 2.93 fb(-1) collected with the BESIII detector at root s = 3.773 GeV. No significant signals are observed, and the corresponding upper limits on the branching fractions at the 90% confidence level are determined. The sensitivities of the results are at the level of 10(-5)-10(-6), providing a large improvement over previous searches.
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| 5. |
- Schmit, Stephanie L, et al.
(författare)
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Novel Common Genetic Susceptibility Loci for Colorectal Cancer.
- 2019
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 111:2, s. 146-157
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Tidskriftsartikel (refereegranskat)abstract
- Background: Previous genome-wide association studies (GWAS) have identified 42 loci (P < 5 × 10-8) associated with risk of colorectal cancer (CRC). Expanded consortium efforts facilitating the discovery of additional susceptibility loci may capture unexplained familial risk.Methods: We conducted a GWAS in European descent CRC cases and control subjects using a discovery-replication design, followed by examination of novel findings in a multiethnic sample (cumulative n = 163 315). In the discovery stage (36 948 case subjects/30 864 control subjects), we identified genetic variants with a minor allele frequency of 1% or greater associated with risk of CRC using logistic regression followed by a fixed-effects inverse variance weighted meta-analysis. All novel independent variants reaching genome-wide statistical significance (two-sided P < 5 × 10-8) were tested for replication in separate European ancestry samples (12 952 case subjects/48 383 control subjects). Next, we examined the generalizability of discovered variants in East Asians, African Americans, and Hispanics (12 085 case subjects/22 083 control subjects). Finally, we examined the contributions of novel risk variants to familial relative risk and examined the prediction capabilities of a polygenic risk score. All statistical tests were two-sided.Results: The discovery GWAS identified 11 variants associated with CRC at P < 5 × 10-8, of which nine (at 4q22.2/5p15.33/5p13.1/6p21.31/6p12.1/10q11.23/12q24.21/16q24.1/20q13.13) independently replicated at a P value of less than .05. Multiethnic follow-up supported the generalizability of discovery findings. These results demonstrated a 14.7% increase in familial relative risk explained by common risk alleles from 10.3% (95% confidence interval [CI] = 7.9% to 13.7%; known variants) to 11.9% (95% CI = 9.2% to 15.5%; known and novel variants). A polygenic risk score identified 4.3% of the population at an odds ratio for developing CRC of at least 2.0.Conclusions: This study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screening.
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| 9. |
- Liu, Wei, et al.
(författare)
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Household renovation before and during pregnancy in relation to preterm birth and low birthweight in China
- 2019
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Ingår i: Indoor Air. - : WILEY. - 0905-6947 .- 1600-0668. ; 29:2, s. 202-214
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Tidskriftsartikel (refereegranskat)abstract
- From October 2010 to April 2012, we conducted a cross-sectional study of associations between household environments and childhood health among preschool children in eight Chinese cities. Here, we analyze associations of early household renovation with preterm birth (PTB), low birthweight (LBW), term low birthweight (Term-LBW), and small for gestational age (SGA). Parents responded to questions about household renovation and their children's gestational age and birthweight. In the multivariate logistic regression analyses, household renovation in the year before pregnancy was significantly associated with LBW (sample size: N = 25 813; adjusted odds ratio (OR) with 95% confidence intervals (CIs): 1.23, 1.01-1.50) and Term-LBW (N = 24 823; 1.29, 1.01-1.67). Household renovation during pregnancy was significantly associated with PTB (N = 25 202; 1.28, 1.01-1.69). These significant associations were also found in the two-level (city-child) logistic regression analyses and in the sensitivity analyses among 21 009 children with complete data in all studied variates. Stronger associations were found in certain subgroups. Our findings indicate that household renovation within one year before pregnancy might be a risk factor for LBW and Term-LBW, while household renovation during pregnancy could be a risk factor for PTB.
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| 10. |
- Qu, Mingqi, et al.
(författare)
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Molecular Genetic and Epigenetic analysis of NCX2/SLC8A2 at 19q13.3 in Human Gliomas
- 2010
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Ingår i: Neuropathology and Applied Neurobiology. - : Wiley. - 0305-1846 .- 1365-2990. ; 36:3, s. 198-210
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Tidskriftsartikel (refereegranskat)abstract
- AimLoss of heterozygosity (LOH) at 19q13.3 is a common genetic change in human gliomas, indicating yet unknown glial-specific tumour suppressor genes in this chromosome region. NCX2/SLC8A2 located on chromosome 19q13.32 encodes a Na(+)/Ca(2+)exchanger, which contributes to intracellular Ca(2+)homeostasis. Its expression is restricted to brain, and it is neither present in other normal tissues nor in gliomas at any significant level. The aim of this study was to investigate if NCX2 might be a tumour suppressor gene involved in glioma.MethodsWe performed a systematic analysis of NCX2 in 42 human gliomas using microsatellite analysis for evaluation of LOH at 19q, DNA sequencing and DNA methylation analysis.ResultsExcept for three known intragenic SNPs, rs12459087, rs7259674, and rs8104926, no NCX2 sequence variations were detected in any of the tumour samples. Furthermore, a CpG island in the 5' promoter region of NCX2 was unmethylated. Interestingly, the CpG sites of three gene-body CpG islands located in exon 2, intron 2-3 and exon 3 and of a 5' CpG rich area relevant to so called CpG island shore of NCX2 were methylated in all 8 glioma samples and in 3 established glioma cell lines tested. Surprisingly, NCX2 could be activated by addition of the DNA methylation inhibitor 5-aza-2'-deoxycytidine to glioma cell lines in which NCX2 was completely silent.ConclusionResults indicate that DNA methylation may play a key role in the transcriptional silencing of NCX2.
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