ABSTRACT
A new short-lived neutron-deficient isotope ^{220}Np was synthesized in the fusion-evaporation reaction ^{185}Re(^{40}Ar,5n)^{220}Np at the gas-filled recoil separator SHANS. Based on the measurement of the correlated α-decay chains, the decay properties of ^{220}Np with E_{α}=10040(18) keV and T_{1/2}=25_{-7}^{+14} µs were determined, which are in good agreement with theoretical predictions. From the new experimental results coupled with the recently reported α-decay data of ^{219,223}Np, the α-decay systematics for Np isotopes around N=126 was established, which allows us for the first time to test the robustness of the N=126 shell closure in Z=93 Np isotopes. The results also indicate that, in the region of nuclei with Z≥83, the proton drip line has been reached for all odd-Z isotopes up to Np.
ABSTRACT
OBJECTIVE: Acute myeloid leukemia (AML) is a bone marrow malignancy. Long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) plays an important role in several cancers. However, the role of lncRNA UCA1 in AML remained unclear. MATERIALS AND METHODS: LncRNA UCA1 expressions in different cell lines were determined by RT-PCR. In human myelogenous leukemia (ML) cell lines K562 and HL60, effects of lncRNA UCA1 knockdown on cell viability, migration, invasion, and apoptosis were assessed, respectively. Binding effects between lncRNA UCA1 and microRNA (miR)-126, and between miR-126 and RAC1 3'UTR were detected by RT-PCR and luciferase activity assay. Involvements of miR-126 and RAC1 in lncRNA UCA1-mediated cell bioactivities were assessed. RESULTS: We found that lncRNA UCA1 was upregulated in ML cell lines. Knockdown of lncRNA UCA1 inhibited cell viability, migration, invasion, and prompted apoptosis of ML cells in vitro. LncRNA UCA1 could bind with miR-126 and downregulate miR-126 expression. Simultaneously, the anti-growth and anti-metastasis actions of lncRNA UCA1 knockdown on ML cells were reversed by miR-126 suppression. RAC1 was a target gene of miR-126, and the anti-ML actions of miR-126 were abolished by RAC1 overexpression. Moreover, PI3K/AKT and JAK/STAT signaling pathways were blocked by miR-126 overexpression while were activated by RAC1 overexpression. CONCLUSIONS: Taken together, this study elucidates a novel UCA1-miR-126-RAC1 regulatory network in ML cells, which may provide the feasibility for use lncRNA-based therapy in AML treatment.
