Influence of C(60) fullerene on the ischemia-reperfusion injury in the skeletal muscle of rat limb: mechanokinetic and biochemical analysis

Influence of the pristine C60 fullerene aqueous colloidal solution (C60FAS) on the ischemia-reperfusion injury in the skeletal muscle of rat limb was studied. Skeletal muscle damage effects were induced by 3 h lasting­ vascular ischemia. The impact of C60FAS was studied after its intramuscular injection immediately after 1 h of reper­fusion at different doses, namely: 1, 2 and 3 mg/kg of body weight. Changes in the mechanokinetic parame­ters of ischemic skeletal muscle contraction at different modes of functioning and biochemical parame­ters of blood were used as markers of ischemic injury, and analyzed in detail under action of C60FAS. The obtained results indicate on great promise of use of C60FAS to reduce the consequences of ischemic muscle trauma

Belle II Technical Design Report

The Belle detector at the KEKB electron-positron collider has collected almost 1 billion Y(4S) events in its decade of operation. Super-KEKB, an upgrade of KEKB is under construction, to increase the luminosity by two orders of magnitude during a three-year shutdown, with an ultimate goal of 8E35 /cm^2 /s luminosity. To exploit the increased luminosity, an upgrade of the Belle detector has been proposed. A new international collaboration Belle-II, is being formed. The Technical Design Report presents physics motivation, basic methods of the accelerator upgrade, as well as key improvements of the detector.Comment: Edited by: Z. Dole\v{z}al and S. Un

First Observation of CP Violation in B0->D(*)CP h0 Decays by a Combined Time-Dependent Analysis of BaBar and Belle Data

We report a measurement of the time-dependent CP asymmetry of B0->D(*)CP h0 decays, where the light neutral hadron h0 is a pi0, eta or omega meson, and the neutral D meson is reconstructed in the CP eigenstates K+ K-, K0S pi0 or K0S omega. The measurement is performed combining the final data samples collected at the Y(4S) resonance by the BaBar and Belle experiments at the asymmetric-energy B factories PEP-II at SLAC and KEKB at KEK, respectively. The data samples contain ( 471 +/- 3 ) x 10^6 BB pairs recorded by the BaBar detector and ( 772 +/- 11 ) x 10^6, BB pairs recorded by the Belle detector. We measure the CP asymmetry parameters -eta_f S = +0.66 +/- 0.10 (stat.) +/- 0.06 (syst.) and C = -0.02 +/- 0.07 (stat.) +/- 0.03 (syst.). These results correspond to the first observation of CP violation in B0->D(*)CP h0 decays. The hypothesis of no mixing-induced CP violation is excluded in these decays at the level of 5.4 standard deviations.Comment: 9 pages, 2 figures, submitted to Physical Review Letter

Measurement of cos⁡2β\cos{2\beta} in B0→D(∗)h0B^{0} \to D^{(*)} h^{0} with D→KS0π+π−D \to K_{S}^{0} \pi^{+} \pi^{-} decays by a combined time-dependent Dalitz plot analysis of BaBar and Belle data

We report measurements of $\sin{2\beta}$ and $\cos{2\beta}$ from a time-dependent Dalitz plot analysis of $B^{0} \to D^{(*)} h^{0}$ with $D \to K_{S}^{0} \pi^{+} \pi^{-}$ decays, where the light unflavored and neutral hadron $h^{0}$ is a $\pi^{0}$, $\eta$, or $\omega$ meson. The analysis is performed with a combination of the final data sets of the \babar\ and Belle experiments containing $471 \times 10^{6}$ and $772 \times 10^{6}$ $B\bar{B}$ pairs collected at the $\Upsilon\left(4S\right)$ resonance at the asymmetric-energy B factories PEP-II at SLAC and KEKB at KEK, respectively. We measure $\sin{2\beta} = 0.80 \pm 0.14 \,(\rm{stat.}) \pm 0.06 \,(\rm{syst.}) \pm 0.03 \,(\rm{model})$ and $\cos{2\beta} = 0.91 \pm 0.22 \,(\rm{stat.}) \pm 0.09 \,(\rm{syst.}) \pm 0.07 \,(\rm{model})$. The result for the direct measurement of the angle is $\beta = \left( 22.5 \pm 4.4 \,(\rm{stat.}) \pm 1.2 \,(\rm{syst.}) \pm 0.6 \,(\rm{model}) \right)^{\circ}$. The last quoted uncertainties are due to the composition of the $D^{0} \to K_{S}^{0} \pi^{+} \pi^{-}$ decay amplitude model, which is newly established by a Dalitz plot amplitude analysis of a high-statistics $e^{+}e^{-} \to c\bar{c}$ data sample as part of this analysis. We find the first evidence for $\cos2\beta>0$ at the level of $3.7$ standard deviations. The measurement excludes the trigonometric multifold solution $\pi/2 - \beta = (68.1 \pm 0.7)^{\circ}$ at the level of $7.3$ standard deviations and therefore resolves an ambiguity in the determination of the apex of the CKM Unitarity Triangle. The hypothesis of $\beta = 0^{\circ}$ is ruled out at the level of $5.1$ standard deviations, and thus CP violation is observed in $B^{0} \to D^{(*)} h^{0}$ decays.Comment: To be submitted to Physical Review

The Physics of the B Factories

This work is on the Physics of the B Factories. Part A of this book contains a brief description of the SLAC and KEK B Factories as well as their detectors, BaBar and Belle, and data taking related issues. Part B discusses tools and methods used by the experiments in order to obtain results. The results themselves can be found in Part C

The Belle II Physics Book

We present the physics program of the Belle II experiment, located on the intensity frontier SuperKEKB $e^+e^-$ collider. Belle II collected its first collisions in 2018, and is expected to operate for the next decade. It is anticipated to collect 50/ab of collision data over its lifetime. This book is the outcome of a joint effort of Belle II collaborators and theorists through the Belle II theory interface platform (B2TiP), an effort that commenced in 2014. The aim of B2TiP was to elucidate the potential impacts of the Belle II program, which includes a wide scope of physics topics: B physics, charm, tau, quarkonium, electroweak precision measurements and dark sector searches. It is composed of nine working groups (WGs), which are coordinated by teams of theorist and experimentalists conveners: Semileptonic and leptonic B decays, Radiative and Electroweak penguins, phi_1 and phi_2 (time-dependent CP violation) measurements, phi_3 measurements, Charmless hadronic B decay, Charm, Quarkonium(like), tau and low-multiplicity processes, new physics and global fit analyses. This book highlights "golden- and silver-channels", i.e. those that would have the highest potential impact in the field. Theorists scrutinised the role of those measurements and estimated the respective theoretical uncertainties, achievable now as well as prospects for the future. Experimentalists investigated the expected improvements with the large dataset expected from Belle II, taking into account improved performance from the upgraded detector.Comment: 689 page

Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council