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A bstract We present the analysis of two-particle angular correlations using coordinate systems defined with the conventional beam axis and the event thrust axis. We propose the latter as a good representation for the correlation structure interpretation in the e + e − collision system. The e + e − collisions to hadronic final states at center-of-mass energies of s = 10 . 52 GeV and 10.58 GeV are recorded by the Belle detector at KEKB. In this paper, results on the first dataset are supplementary to the previous Belle publication [ 1 ]. At the same time, the latter is the first two-particle correlation measurement at collision energy on the Υ (4 S ) resonance and is sensitive to its decay products. Measurements are reported as a function of the charged-particle multiplicity. Finally, a qualitative understanding of the correlation structure is discussed using a combination of Monte Carlo simulations and experimental data.

A bstract The first dedicated search for the η c 2 (1 D ) is carried out using the decays B + → η c 2 (1 D ) K + , B 0 → η c 2 (1 D ) K S 0 , B 0 → η c 2 (1 D ) π − K + , and B + → η c 2 (1 D ) π + K S 0 with η c 2 (1 D ) → h c γ . No significant signal is found. For the η c 2 (1 D ) mass range between 3795 and 3845 MeV /c 2 , the branching-fraction upper limits are determined to be ℬ( B + → η c 2 (1 D ) K + ) × ℬ( η c 2 (1 D ) → h c γ ) < 3 . 7 × 10 − 5 , ℬ( B 0 → η c 2 (1 D ) K 0 ) × ℬ( η c 2 (1 D ) → h c γ ) < 3 . 5 × 10 − 5 , ℬ( B 0 → η c 2 (1 D ) π − K + ) × ℬ( η c 2 (1 D ) → h c γ ) < 1 . 0 × 10 − 4 , and ℬ( B + → η c 2 (1 D ) π + K S 0 ) × ℬ( η c 2 (1 D ) → h c γ ) < 1 . 1 × 10 − 4 at 90% C.L. The analysis is based on the 711 fb − 1 data sample collected on the ϒ(4 S ) resonance by the Belle detector, which operated at the KEKB asymmetric-energy e + e − collider.

A bstract We present measurements of the branching fractions for the decays B → Kμ + μ − and B → Ke + e − , and their ratio ( R K ), using a data sample of 711 fb − 1 that contains 772 × 10 6 B B ¯ events. The data were collected at the ϒ(4 S ) resonance with the Belle detector at the KEKB asymmetric-energy e + e − collider. The ratio R K is measured in five bins of dilepton invariant-mass-squared ( q 2 ): q 2 ∈ (0 . 1 , 4 . 0) , (4 . 00 , 8 . 12) , (1 . 0 , 6 . 0), (10 . 2 , 12 . 8) and ( > 14 . 18) GeV 2 /c 4 , along with the whole q 2 region. The R K value for q 2 ∈ (1 . 0 , 6 . 0) GeV 2 /c 4 is 1.03 − 0.24 + 0.28 ± 0 . 01. The first and second uncertainties listed are statistical and systematic, respectively. All results for R K are consistent with Standard Model predictions. We also measure CP -averaged isospin asymmetries in the same q 2 bins. The results are consistent with a null asymmetry, with the largest difference of 2.6 standard deviations occurring for the q 2 ∈ (1 . 0 , 6 . 0) GeV 2 /c 4 bin in the mode with muon final states. The measured differential branching fractions, d ℬ /dq 2 , are consistent with theoretical predictions for charged B decays, while the corresponding values are below the expectations for neutral B decays. We have also searched for lepton-flavor-violating B → Kμ ± e ∓ decays and set 90% confidence-level upper limits on the branching fraction in the range of 10 − 8 for B + → K + μ ± e ∓ , and B 0 → K 0 μ ± e ∓ modes.

Low oxygen tension influences tumor progression by enhancing angiogenesis; and histone deacetylases (HDAC) are implicated in alteration of chromatin assembly and tumorigenesis. Here we show induction of HDAC under hypoxia and elucidate a role for HDAC in the regulation of hypoxia-induced angiogenesis. Overexpressed wild-type HDAC1 downregulated expression of p53 and von Hippel–Lindau tumor suppressor genes and stimulated angiogenesis of human endothelial cells. A specific HDAC inhibitor, trichostatin A (TSA), upregulated p53 and von Hippel–Lindau expression and downregulated hypoxia-inducible factor-1α and vascular endothelial growth factor. TSA also blocked angiogenesis in vitro and in vivo . TSA specifically inhibited hypoxia-induced angiogenesis in the Lewis lung carcinoma model. These results indicate that hypoxia enhances HDAC function and that HDAC is closely involved in angiogenesis through suppression of hypoxia-responsive tumor suppressor genes.

Background:Systemic Lupus Erythematosus (SLE) is a multifaceted autoimmune disorder characterized by diverse clinical manifestations. Despite improved survival rates, the mortality risk in SLE patients remains elevated compared to the general population.Objectives:We aimed to evaluate all-cause and cause-specific mortality risks in Korean patients with SLE, stratified by age and gender. Additionally, the impact of medications and comorbidities on mortality risk was investigated.Methods:Using data from the National Health Insurance database spanning 2008 to 2018, incident SLE patients aged 10-79 years were included. The primary endpoint was all-cause death and cause-specific death, with secondary outcomes focusing on cause-specific death stratified by age group. The main causes of death were identified using the ICD-10 code of the primary diagnosis within six months prior to death. The mortality rate (MR) was calculated as the number of deaths per 100,000 person-years (PYs). A generalized estimating equations model was employed for risk factor analysis.Results:A total of 11,375 incident SLE patients were recruited, with an average age of 42.3 ± 16.7 years and 86.1% female. During 57,658 PYs of observation, 728 deaths occurred, resulting in an MR of 1,262.62 per 100,000 PYs. The MR for males (2,718.86/100,000 PYs) exceeded that for females (1,060.57/100,000 PYs). SLE itself (381.56/100,000 PYs) was the leading cause of death, followed by cardiovascular disease (202.92/100,000 PYs), cancer (175.17/100,000 PYs), infection (143.95/100,000 PYs), and renal disease (57.23/100,000 PYs). Age-specific mortality risk increased proportionally with both age and mortality risk. Among adolescents (10-19 years), all-cause MR was 520.47 per 100,000 PYs, with SLE itself accounting for over half of the cause of deaths. In elderly patients (70-79 years), all-cause mortality peaked at 7,252.06 per 100,000 PYs, emphasizing the impact of infection and cancer. Risk factor analysis for SLE-related mortality revealed significant associations with comorbidities (Table 2). Pulmonary alveolar hemorrhage (Hazard Ratio [HR] 9.93, 95% CI 3.81-25.89), pulmonary arterial hypertension (HR 3.77, 95% CI 1.54-9.21), and interstitial lung disease (HR 3.27, 95% CI 1.87-5.72) were identified as associated factors for mortality in Korean SLE patients. Medications were also associated with increased mortality risk; intravenous glucocorticoids (HR 16.38, 95% CI 10.06-26.66) and cyclophosphamide (HR 5.51, 95% CI 3.38-8.97) were linked to mortality risk in SLE.Conclusion:This study offers a comprehensive analysis of the mortality patterns in Korean SLE patients. SLE itself, cardiovascular disease, cancer, and infection emerged as the primary causes of death, with age at onset influencing mortality patterns. Pulmonary manifestations, intravenous glucocorticoids, and cyclophosphamide were significantly associated with an increased risk of mortalityREFERENCES:NIL.Acknowledgements:NIL.Disclosure of Interests:None declared.

Background:Systemic Lupus Erythematosus (SLE) is a multifaceted autoimmune disorder characterized by diverse clinical manifestations. Despite improved survival rates, the mortality risk in SLE patients remains elevated compared to the general population.Objectives:To evaluate the patterns of mortality and associated risk factors in Korean patients with SLE.Methods:Using data from the National Health Insurance database spanning 2008 to 2018, incident SLE patients aged 10-79 years were included. The primary endpoint was all-cause death and cause-specific death, with secondary outcomes focusing on cause-specific death stratified by age group. The main causes of death were identified using the ICD-10 code of the primary diagnosis within six months prior to death. The mortality rate (MR) was calculated as the number of deaths per 100,000 person-years (PYs). A generalized estimating equations model was employed for risk factor analysis.Results:A total of 11,375 incident SLE patients were recruited, with an average age of 42.3 ± 16.7 years and 86.1% female. During 57,658 PYs of observation, 728 deaths occurred, resulting in an MR of 1,262.62 per 100,000 PYs. The MR for males (2,718.86/100,000 PYs) exceeded that for females (1,060.57/100,000 PYs). SLE itself (381.56/100,000 PYs) was the leading cause of death, followed by cardiovascular disease (202.92/100,000 PYs), cancer (175.17/100,000 PYs), infection (143.95/100,000 PYs), and renal disease (57.23/100,000 PYs). Age-specific mortality risk increased proportionally with both age and mortality risk. Among adolescents (10-19 years), all-cause MR was 520.47 per 100,000 PYs, with SLE itself accounting for over half of the cause of deaths. In elderly patients (70-79 years), all-cause mortality peaked at 7,252.06 per 100,000 PYs, emphasizing the impact of infection and cancer. Risk factor analysis for SLE-related mortality revealed significant associations with comorbidities (Table 1). Pulmonary alveolar hemorrhage (Hazard Ratio [HR] 9.93, 95% CI 3.81-25.89), pulmonary arterial hypertension (HR 3.77, 95% CI 1.54-9.21), and interstitial lung disease (HR 3.27, 95% CI 1.87-5.72) were identified as associated factors for mortality in Korean SLE patients. Medications were also associated with increased mortality risk; intravenous glucocorticoids (HR 16.38, 95% CI 10.06-26.66) and cyclophosphamide (HR 5.51, 95% CI 3.38-8.97) were linked to mortality risk in SLE.Conclusion:This study offers a comprehensive analysis of the mortality patterns in Korean SLE patients. SLE itself, cardiovascular disease, cancer, and infection emerged as the primary causes of death, with age at onset influencing mortality patterns. Pulmonary manifestations, intravenous glucocorticoids, and cyclophosphamide were significantly associated with an increased risk of mortality.Figure 1.All-cause and cause-specific mortality rate stratified by age groupTable 1.Risk factors for SLE-related mortalityVariablesUnivariable HR(95% CI)PMultivariable HR*(95% CI)PSLE-related comorbidities† Opportunistic infection4.41 (3.11, 6.27)< 0.0012.10 (1.37, 3.24)< 0.001 Antiphospholipid antibody syndrome0.71 (0.26, 1.91)0.5000.54 (0.20, 1.44)0.218Avascular necrosis1.00 (0.37, 2.69)0.9971.27 (0.46, 3.47)0.643Interstitial lung disease5.34 (3.51, 8.14)< 0.0013.27 (1.87, 5.72)< 0.001Pulmonary artery hypertension8.87 (4.70, 16.76)< 0.0013.77 (1.54, 9.21)0.004Pulmonary alveolar hemorrhage54.86 (29.49, 102.04)< 0.0019.93 (3.81, 25.89)< 0.001Congestive heart failure7.79 (5.69, 10.65)< 0.0013.06 (1.83, 5.14)< 0.001Lupus nephritis4.58 (3.44, 6.10)< 0.0012.15 (1.46, 3.18)< 0.001Medication††Oral glucocorticoid0.88 (0.68, 1.15)0.3560.64 (0.44, 0.93)0.018IV glucocorticoid19.34 (12.13, 30.85)< 0.00116.38 (10.06, 26.66)< 0.001Hydroxychloroquine0.39 (0.30, 0.51)< 0.0010.39 (0.28, 0.56)< 0.001Nonsteroidal anti-inflammatory drug0.36 (0.25, 0.52)< 0.0010.32 (0.22, 0.49)< 0.001Oral immunosuppressive agents0.64 (0.46, 0.87)0.0050.35 (0.23, 0.54)< 0.001IV cyclophosphamide14.32 (10.58, 19.39)< 0.0015.51 (3.38, 8.97)< 0.001*Adjusted for age, gender, payer type and comorbidities.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of Interests:None declared.

A bstract We report a measurement of the electric dipole moment of the τ lepton ( dτ ) using an 833 fb − 1 data sample collected near the Υ(4 S ) resonance, with the Belle detector at the KEKB asymmetric-energy e + e − collider. Using an optimal observable method, we obtain the real and imaginary parts of d τ as Re( d τ ) = ( − 0 . 62 ± 0 . 63) × 10 − 17 e cm and Im( d τ ) = ( − 0 . 40 ± 0 . 32) × 10 − 17 e cm, respectively. These results are consistent with null electric dipole moment at the present level of experimental sensitivity and improve the sensitivity by about a factor of three.

BackgroundPatients with systemic lupus erythematosus (SLE) have increased mortality related to cardiovascular disease (CVD) and the age is one of important risk factors for the development of CVDs. However, the comparative risk of CVDs in patients with older onset SLE has not been well studied.ObjectivesThis study aims to compare the CVD risk in patients with SLE occurred after the age of 40 compared to those with DM.MethodsIncident SLE patients aged over 40 years and age-sex matched (1:4:4) controls with DM or general population were identified from the nationwide claims database in Korea between 2008 and 2018. We defined CVD risk as ischemic heart disease, stroke, and cardiac death. The incidence rates (IR) and incidence rate ratio (IRR), and adjusted hazard ratio (HR) of CVDs were calculated using generalized estimating equation models.ResultsWe identified 4,272 SLE, 17,003 DM, and 17,088 general population patients aged over 40 years. Their mean age was 53.1 (±9.7) and 81.7% of them were female. The IR per 1,000 person-years (PYs) of CVDs for SLE, DM, and general population were 16.8, 11.7, and 5.7, respectively. Compared to general population, patients with SLE (IRR 3.27, 95% CI 2.78-3.85) and DM (IRR 2.77, 95% CI 2.02-2.56) showed higher CVD risk compared to general population. Increased risk of CVDs in SLE patients was highest in their forties (IRR 4.13, 95% CI 3.06, 5.59). After adjusting confounders, the CVD risk of SLE (HR 1.99, 95% CI 1.66-2.38) was higher than DM (HR 1.39, 95% CI 1.22-1.58) patients.ConclusionOlder onset SLE patients had increased CVD risk compared to general population. Even after adjustment for confounders, SLE patients showed higher CVD risk than DM patients in Korea.AcknowledgementsThis research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HI19C1202).Disclosure of InterestsNone Declared.

A bstract Using data samples of 983.0 fb − 1 and 427.9 fb − 1 accumulated with the Belle and Belle II detectors operating at the KEKB and SuperKEKB asymmetric-energy e + e − colliders, singly Cabibbo-suppressed decays Ξ c + → p K S 0 , Ξ c + → Λ π + , and Ξ c + → Σ 0 π + are observed for the first time. The ratios of branching fractions of Ξ c + → p K S 0 , Ξ c + → Λ π + , and Ξ c + → Σ 0 π + relative to that of Ξ c + → Ξ − π + π + are measured to be B Ξ c + → p K S 0 B Ξ c + → Ξ − π + π + = 2.47 ± 0.16 ± 0.07 % , B Ξ c + → Λ π + B Ξ c + → Ξ − π + π + = 1.56 ± 0.14 ± 0.09 % , B Ξ c + → Σ 0 π + B Ξ c + → Ξ − π + π + = 4.13 ± 0.26 ± 0.22 % . Multiplying these values by the branching fraction of the normalization channel, B Ξ c + → Ξ − π + π + = 2.9 ± 1.3 % , the absolute branching fractions are determined to be B Ξ c + → p K S 0 = 7.16 ± 0.46 ± 0.20 ± 3.21 × 10 − 4 , B Ξ c + → Λ π + = 4.52 ± 0.41 ± 0.26 ± 2.03 × 10 − 4 , B Ξ c + → Σ 0 π + = 1.20 ± 0.08 ± 0.07 ± 0.54 × 10 − 3 . The first and second uncertainties above are statistical and systematic, respectively, while the third ones arise from the uncertainty in B Ξ c + → Ξ − π + π + .

A bstract Charged-lepton-flavor-violation is predicted in several new physics scenarios. We update the analysis of τ lepton decays into a light charged lepton ( ℓ = e ± or μ ± ) and a vector meson ( V 0 = ρ 0 , ϕ , ω , K *0 , or K ¯ *0 ) using 980 fb − 1 of data collected with the Belle detector at the KEKB collider. No significant excess of such signal events is observed, and thus 90% credibility level upper limits are set on the τ → ℓV 0 branching fractions in the range of (1.7–4 . 3) × 10 − 8 . These limits are improved by 30% on average from the previous results.