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In this work, we study the (S, P and D)-wave K + K - contributions to B → K K K decays in the perturbative QCD approach at leading order. Within the two-meson wave functions describing the nonperturbative dynamics in the kaon-pair for different waves, we calculate the branching fractions and the direct CP asymmetries of these decay modes in the corresponding resonance regions. Most of our numerical results are well consistent with the current measurements. We note that the narrow-width approximation is invalid in the quasi-two-body decays B → K f 0 (980) → K K K . For other decays, under the narrow-width approximation we can extract the branching fractions of the corresponding two-body decays involving the intermediate resonant states, and the related branching fractions agree with the current experimental data well. Furthermore, we also predict the branching fractions of the corresponding quasi-two-body decays B → K π + π - , which are expected to be tested in the ongoing LHCb and Belle-II experiments. [ABSTRACT FROM AUTHOR]

Motivated by the observations of the decays B 0 → K 0 ∗ (1430) 0 f 0 (980) and B 0 → K 2 ∗ (1430) 0 f 0 (980) from BaBar collaboration, we study the B 0 (+) → K 0 , 2 ∗ (1430) 0 (+) f 0 (980) / σ decays in the perturbative QCD approach for the first time. In the absence of reliable nonperturbative wave functions we only assume the scalar meson f 0 (980) and σ are two-quark ground states. In our calculations, these decays are all dominated by the hard-scattering emission and annihilation diagrams, while the factorizable emission diagrams are forbidden or suppressed heavily by the vector decay constants. Furthermore, the branching fractions are sensitive to the mixing between f 0 (980) and σ . Comparing our results with the experimental data, a large mixing angle θ is favored. Taking θ = 145 ∘ , the orders of branching fractions of B → K 0 ∗ (1430) 0 σ , B → K 2 ∗ (1430) 0 σ and B → K 0 , 2 ∗ (1430) 0 f 0 (980) are predicted to be 10 - 4 , 10 - 5 and 10 - 6 , respectively, which can be measured in the current experiments such as LHCb and Belle-2. In addition, although these decays are penguin dominant, the mixing also leads to large direct CP asymmetries in these decays. With the precise data in future, our results could shed light on the inner structure of the scalar mesons and can be used to determine the mixing angle of the σ - f 0 (980) system. [ABSTRACT FROM AUTHOR]

Objective: Explore the effects of Astragaloside IV and Scorpion Venom Peptide on the activity, migration, apoptosis, cell cycle, autophagy, and the expression of proteins related to the PI3K/AKT signaling pathway in prostate cancer cells., Methods: The human prostate cancer cell lines LNCaP and PC-3 were randomly divided into blank control group, Astragaloside IV group, Scorpion Venom Peptide group, Astragaloside IV-Scorpion Venom Peptide group, and rapamycin (positive drug group). After corresponding drug treatments for 24 hours, logarithmic growth phase tumor cells were collected for testing. Cell proliferation was assessed using a Cell Counting Kit-8 (CCK-8) assay, Transwell assay, apoptosis assay, cell cycle assay, and immunofluorescence analysis were performed to detect the activity and migration capacity of prostate cancer cells in each group, as well as their effects on apoptosis, cell cycle, and the autophagy target LC3. Western blot analysis was employed to measure the protein expression levels of p-PI3K, p-Akt, p-mTOR, Beclin1, LC3, and P62., Results: Compared to the blank control group, the Astragaloside IV-Scorpion Venom Peptide group exhibited a significant decrease in the activity of prostate cancer cells (P<0.05) and a reduction in the cell invasion ability (migration capacity) (P<0.05). The early apoptosis rate (LR), late apoptosis rate (UR), and total apoptosis rate all increased (P<0.05). The proportion of cells in the G1 phase increased (P<0.05), while the proportion in the G2+S phase decreased (P<0.05). The immunofluorescence expression of LC3 significantly increased (P<0.05). The expression of LC3Ⅱ and Beclin1 proteins in prostate cancer cells LNCaP and PC-3 was upregulated (P<0.05), while the expression of P62, p-PI3K, p-AKT, and p-mTOR proteins was downregulated (P<0.05).Astragaloside IV-Scorpion Venom Peptide is superior to the Astragaloside IV group or Scorpion Venom Peptide group alone in inhibiting the activity and migration capacity of prostate cancer cells, suppressing cell mitosis, promoting early apoptosis, upregulating the expression level of LC3, and inhibiting the PI3K/AKT pathway while promoting autophagy (P<0.05)., Conclusion: The mechanism by which Astragaloside IV-Scorpion Venom Peptide inhibits the proliferation and migration of prostate cancer cells, suppresses cell mitosis, promotes early apoptosis, and enhances autophagy may be related to the inhibition of the PI3K/AKT pathway.