Search for: All records

We report measurements of production cross sections for ${\rho }^{+}$, ${\rho }^0$, $\omega$, $K^{*+}$, $K^{*0}$, $\varphi$, $\eta$, $K_S^0$, $f_0\left(980\right)$, $D^{+}$, $D^0$, $D_s^{+}$, $D^{*+}$, $D^{*0}$, and $D_s^{*+}$in $e^{+}{e}^{-}$collisions at a center-of-mass energy near 10.58 GeV. The data were recorded by the Belle experiment, consisting of $571{\mathrm{fb}}^{-1}$at 10.58 GeV and $74{\mathrm{fb}}^{-1}$at 10.52 GeV. Production cross sections are extracted as a function of the fractional hadron momentum $x_p$. The measurements are compared to Monte Carlo generator predictions with various fragmentation settings, including those that have increased fragmentation into vector mesons over pseudoscalar mesons. The cross sections measured for light hadrons are consistent with no additional increase of vector over pseudoscalar mesons. The charmed-meson cross sections are compared to earlier measurements—when available—including older Belle results, which they supersede. They are in agreement before application of an improved initial-state radiation correction procedure that causes slight changes in their $x_p$shapes. Published by the American Physical Society2025 

NKX3.1’s downregulation is strongly associated with prostate cancer (PCa) initiation, progression, and CRPC development. Nevertheless, a clear disagreement exists between NKX3.1 protein and mRNA levels in PCa tissues, indicating that its regulation at a post-translational level plays a vital role. This study identified a strong negative relationship between NKX3.1 and LIMK2, which is critical in CRPC pathogenesis. We identified that NKX3.1 degradation by direct phosphorylation by LIMK2 is crucial for promoting oncogenicity in CRPC cells and in vivo. LIMK2 also downregulates NKX3.1 mRNA levels. In return, NKX3.1 promotes LIMK2’s ubiquitylation. Thus, the negative crosstalk between LIMK2-NKX3.1 regulates AR, ARv7, and AKT signaling, promoting aggressive phenotypes. We also provide a new link between NKX3.1 and PTEN, both of which are downregulated by LIMK2. PTEN loss is strongly linked with NKX3.1 downregulation. As NKX3.1 is a prostate-specific tumor suppressor, preserving its levels by LIMK2 inhibition provides a tremendous opportunity for developing targeted therapy in CRPC. Further, as NKX3.1 downregulates AR transcription and inhibits AKT signaling, restoring its levels by inhibiting LIMK2 is expected to be especially beneficial by co-targeting two driver pathways in tandem, a highly desirable requisite for developing effective PCa therapeutics. 

We measure the branching fraction and $CP$-violating flavor-dependent rate asymmetry of $B^0\to {\pi }^0{\pi }^0$decays reconstructed using the Belle II detector in an electron-positron collision sample containing $387\times {10}^6\mathrm{\Upsilon }\left(4S\right)$mesons. Using an optimized event selection, we find $125\pm 20$signal decays in a fit to background-discriminating and flavor-sensitive distributions. The resulting branching fraction is $(1.25\pm 0.23)\times {10}^{-6}$and the $CP$-violating asymmetry is $0.03\pm 0.30$. Published by the American Physical Society2025 

A<sc>bstract</sc> We report measurements of the absolute branching fractions$$\mathcal{B}\left({B}_{s}^{0}\to {D}_{s}^{\pm }X\right)$$,$$\mathcal{B}\left({B}_{s}^{0}\to {D}^{0}/{\overline{D} }^{0}X\right)$$, and$$\mathcal{B}\left({B}_{s}^{0}\to {D}^{\pm }X\right)$$, where the latter is measured for the first time. The results are based on a 121.4 fb⁻¹data sample collected at the Υ(10860) resonance by the Belle detector at the KEKB asymmetric-energye⁺e⁻collider. We reconstruct one$${B}_{s}^{0}$$meson in$${e}^{+}{e}^{-}\to \Upsilon\left(10860\right)\to {B}_{s}^{*}{\overline{B} }_{s}^{*}$$events and measure yields of$${D}_{s}^{+}$$,D⁰, andD⁺mesons in the rest of the event. We obtain$$\mathcal{B}\left({B}_{s}^{0}\to {D}_{s}^{\pm }X\right)=\left(68.6\pm 7.2\pm 4.0\right)\%$$,$$\mathcal{B}\left({B}_{s}^{0}\to {D}^{0}/{\overline{D} }^{0}X\right)=\left(21.5\pm 6.1\pm 1.8\right)\%$$, and$$\mathcal{B}\left({B}_{s}^{0}\to {D}^{\pm }X\right)=\left(12.6\pm 4.6\pm 1.3\right)\%$$, where the first uncertainty is statistical and the second is systematic. Averaging with previous Belle measurements gives$$\mathcal{B}\left({B}_{s}^{0}\to {D}_{s}^{\pm }X\right)=\left(63.4\pm 4.5\pm 2.2\right)\%$$and$$\mathcal{B}\left({B}_{s}^{0}\to {D}^{0}/{\overline{D} }^{0}X\right)=\left(23.9\pm 4.1\pm 1.8\right)\%$$. For the$${B}_{s}^{0}$$production fraction at the Υ(10860), we find$${f}_{s}=\left({21.4}_{-1.7}^{+1.5}\right)\%$$. 

The first measurements of proton emission accompanied by neutron emission in the electromagnetic dissociation (EMD) of ${}^{208}\mathrm{Pb}$nuclei in the ALICE experiment at the Large Hadron Collider are presented. The EMD protons and neutrons emitted at very forward rapidities are detected by the proton and neutron zero degree calorimeters of the ALICE experiment. The emission cross sections of zero, one, two, and three protons accompanied by at least one neutron were measured in ultraperipheral ${}^{208}\mathrm{Pb}\text{−}{}^{208}\mathrm{Pb}$collisions at a center-of-mass energy per nucleon pair $\sqrt{s_{NN}}=5.02\mathrm{TeV}$. The 0p and 3p cross sections are described by the RELDIS model within their measurement uncertainties, while the 1p and 2p cross sections are underestimated by the model by 17–25%. According to this model, these 0p, 1p, 2p, and 3p cross sections are associated, respectively, with the production of various isotopes of Pb, Tl, Hg, and Au in the EMD of ${}^{208}\mathrm{Pb}$. The cross sections of the emission of a single proton accompanied by the emission of one, two, or three neutrons in EMD were also measured. The data are significantly overestimated by the RELDIS model, which predicts that the (1p,1n), (1p,2n), and (1p,3n) cross sections are very similar to the cross sections for the production of the thallium isotopes ${}^{206,205,204}\mathrm{Tl}$. ©2025 CERN, for the ALICE Collaboration2025CERN