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In this work, al atent energy-transfer process in traditional Eu 3 + ,Tb 3 + -doped phosphorsi sp roposed and a new class of Eu 3 + ,Tb 3 + -doped Na 4 CaSi 3 O 9 (NCSO) phosphors is presentedw hich is enabled by luminescence decay dynamics that optimize the electron-transfer energy process. Relative to other Eu 3 + ,Tb 3 + -doped phosphors, the as-synthesized Eu 3 + ,Tb 3 + -doped NCSO phosphors show improved large-scale tunable emission color from green to red upon UV excitation,c ontrolled by the Tb 3 + /Eu 3 + doping ratio. Detailed spectroscopicm easurements in the vacuum ultraviolet (VUV)/UV/Vis region were used to determine the Eu 3 + -O 2À charge-transfer energy,4 f-5d transition energies, andt he energies of 4f excited multiplets of Eu 3 + and Tb 3 + with different 4f N electronic configurations. The Tb 3 + !Eu 3 + energy-transfer pathway in the co-doped sample was systematically investigated, by employing luminescence decay dynamics analysist oe lucidate the relevant energy-transfer mechanism in combination with the appropriate model simulation. To demonstrate their application potential, ap rototypew hitelight-emitting diode (WLED) device was successfully fabricated by using the yellow luminescence NCSO:0.03Tb 3 + , 0.05Eu 3 + phosphor with high thermal stabilitya nd aB a-MgAl 10 O 17 :Eu 2 + phosphor in combination with an ear-UV chip. These findings open up an ew avenuet or ealize and develop multifunctional high-performancep hosphors by manipulating the energy-transfer process forp ractical applications.

Hepatocellular carcinoma (HCC) initiated by hepatitis B virus (HBV) infection is a complicated process. MiR‐155 can alter the immune microenvironment to affect the host's anti‐infective ability. This study investigated the mechanism by which miR‐155 affects tumour‐associated macrophage (TAM) polarization at a molecular level, thus affecting the malignant progression of HBV+HCC. MiR‐155 and TAM‐related cytokine expression were analysed by qRT‐PCR. The distribution of TAMs was detected by immunohistochemistry. The effect of the aberrant miR‐155 expression on macrophage polarization was examined by flow cytometry. The targeted relationship was verified by dual‐luciferase assay, and the protein level of src homology 2 domain‐containing inositol polyphosphate 5‐phosphatase 1 (SHIP1) was detected by western blot. The proliferation of HCC cells was examined by CCK‐8 and colony formation assays. Invasion and migration of HCC cells were detected by transwell assay. In HBV+HCC tissues, miR‐155 was significantly highly expressed and the number of CD206‐positive TAM (CD206+ TAM) and CD68‐positive TAM (CD68+ TAM) were higher than those in HBV−HCC tissues. In addition, miR‐155 overexpression significantly promoted M2‐type macrophage polarization, whilst miR‐155 silencing expression significantly promoted M1‐type macrophage polarization. Besides, the miR‐155/SHIP1 axis accelerated HCC cell invasion, proliferation and migration by inducing M2‐type macrophage polarization. MiR‐155 accelerates HCC cell proliferation, migration and invasion by targeting SHIP1 expression and inducing macrophage M2 polarization. This finding provides new insights into the development of novel therapeutic strategies for combatting HBV+HCC and a new reference for exploring anti‐tumour immunotherapy.

A novel porous Cd(ii) metal–organic framework (MOF) with the chemical composition of {[H3O][Cd(bci)]} n ·2n(H2O) (1, H3bci = bis(2-carboxyethyl)isocyanurate) was prepared via hydrothermal responses of H3bci and Cd(NO3)2·4H2O. Luminescent property investigations indicated that compound 1 had high sensitivity toward Fe3+, and the detection limit of Fe3+ was as low as 2.15 × 10−4 M. The application values of Fe3+ on Hepatitis B were assessed, and its associated mechanism was identified simultaneously. First, the cytotoxic mediator (TNF-α) substance released into plasma was measured through the ELISA. In addition, real-time RT-PCR was employed to determine the Hepatitis B viral replication gene relative expression levels. Finally, the novel compound’s toxicity against human normal liver cells was tested by using the CCK-8 assay.