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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. 

Abstract Despite the f₀(980) hadron having been discovered half a century ago, the question about its quark content has not been settled: it might be an ordinary quark-antiquark ($${{\rm{q}}}\overline{{{\rm{q}}}}$$ $q\overline{q}$) meson, a tetraquark ($${{\rm{q}}}\overline{{{\rm{q}}}}{{\rm{q}}}\overline{{{\rm{q}}}}$$ $q\overline{q}q\overline{q}$) exotic state, a kaon-antikaon ($${{\rm{K}}}\overline{{{\rm{K}}}}$$ $K\overline{K}$) molecule, or a quark-antiquark-gluon ($${{\rm{q}}}\overline{{{\rm{q}}}}{{\rm{g}}}$$ $q\overline{q}g$) hybrid. This paper reports strong evidence that the f₀(980) state is an ordinary$${{\rm{q}}}\overline{{{\rm{q}}}}$$ $q\overline{q}$meson, inferred from the scaling of elliptic anisotropies (v₂) with the number of constituent quarks (n_q), as empirically established using conventional hadrons in relativistic heavy ion collisions. The f₀(980) state is reconstructed via its dominant decay channel f₀(980) →π⁺π⁻, in proton-lead collisions recorded by the CMS experiment at the LHC, and itsv₂is measured as a function of transverse momentum (p_T). It is found that then_q= 2 ($${{\rm{q}}}\overline{{{\rm{q}}}}$$ $q\overline{q}$state) hypothesis is favored overn_q= 4 ($${{\rm{q}}}\overline{{{\rm{q}}}}{{\rm{q}}}\overline{{{\rm{q}}}}$$ $q\overline{q}q\overline{q}$or$${{\rm{K}}}\overline{{{\rm{K}}}}$$ $K\overline{K}$states) by 7.7, 6.3, or 3.1 standard deviations in thep_T< 10, 8, or 6 GeV/cranges, respectively, and overn_q= 3 ($${{\rm{q}}}\overline{{{\rm{q}}}}{{\rm{g}}}$$ $q\overline{q}g$hybrid state) by 3.5 standard deviations in thep_T< 8 GeV/crange. This result represents the first determination of the quark content of the f₀(980) state, made possible by using a novel approach, and paves the way for similar studies of other exotic hadron candidates. 

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