[en] To evaluate ¹²⁵I labeled recombinant macrophage migration inhibitory factors (rMIF) for the scintigraphic imaging of inflammation, rMIF was labeled with ¹²⁵I by Iodo- gen method. ¹²⁵I-rMIF was isolated by Sephadex G25 column. The stability, immune specificity of ¹²⁵I-rMIF and its biodistribution in inflammatory model of mice were studied. The labeling yield of ¹²⁵I-rMIF was 96.5%. It was stable within 48 h at room temperature. The biodistribution results showed that the ¹²⁵I-rMIF was metabolized by the liver, the radioactivity clearance mainly happened in the kidney and the speed of the blood clearance was rapid. After caudal vein iniection with ¹²⁵I-rMIF, the ratio of radioactivity uptake between inflammatory limb (target) and contra lateral healthy limb (non target)(T/NT) were 1.42, 1.35, 2.18 and 2.05 at 0.5, 1, 6, 24 h respectively. ¹²⁵I-rMIF had the capability of locating the inflammatory foci. The advance of it is more obviously at the late stage than that at the early stage. ¹²⁵I-rMIF may be a potential agent for the diagnosis of concealed and subacute inflammatory disease. (authors)

[en] Graphical abstract: MnCO3 microcrystals with hierarchical superstructures were synthesized by using the CO2 in atmosphere as carbonate ions source and Schiff base as shape guiding-agent in water/ethanol system under hydrothermal condition. Highlights: → The most interesting in this work is the use of the greenhouse gases CO₂ in atmosphere as carbonate ions source to precipitate with Mn²⁺ for producing MnCO₃ crystals. → This work is the first report related to the small organic molecule Schiff base as shape guiding-agent to produce different MnCO₃ hierarchical superstructures. → We are controllable synthesis of the MnCO₃ hierarchical superstructures such as chrysanthemum, straw-bundle, dumbbell and sphere-like microcrystals. → The as-prepared MnCO₃ could be used precursor to fabricate the Mn₂O₃ hierarchical superstructures after thermal decomposition at high temperature. -- Abstract: MnCO₃ with hierarchical superstructures such as chrysanthemum, straw-bundle, dumbbell and sphere-like were synthesized in water/ethanol system under environment-friendly hydrothermal condition. In the synthesis process, the CO₂ in atmosphere was used as the source of carbonate ions and Schiff base was used as shape guiding-agent. The different superstructures of MnCO₃ could be obtained by controlling the hydrothermal temperature, the molar ratio of manganous ions to the Schiff base, or the volume ratio of water to ethanol. A tentative growth mechanism for the generation of MnCO₃ superstructures was proposed based on the rod-dumbbell-sphere model. Furthermore, the MnCO₃ as precursor could be further successfully transferred to Mn₂O₃ microstructure after heating in the atmosphere at 500 ^oC, and the morphology of the Mn₂O₃ was directly determined by that of the MnCO₃ precursor.

[en] To investigate the effects of CAL-101, particularly when combined with bortezomib (BTZ) on mantle cell lymphoma (MCL) cells, and to explore its relative mechanisms. MTT assay was applied to detect the inhibitory effects of different concentrations of CAL-101. MCL cells were divided into four groups: control group, CAL-101 group, BTZ group, and CAL-101/BTZ group. The expression of PI3K-p110σ, AKT, ERK, p-AKT and p-ERK were detected by Western blot. The apoptosis rates of CAL-101 group, BTZ group, and combination group were detected by flow cytometry. The location changes of nuclear factor kappa-B (NF-κB) of 4 groups was investigated by NF-κB Kit exploring. Western blot was applied to detect the levels of caspase-3 and the phosphorylation of AKT in different groups. CAL-101 dose- and time-dependently induced reduction in MCL cell viability. CAL-101 combined with BTZ enhanced the reduction in cell viability and apoptosis. Western blot analysis showed that CAL-101 significantly blocked the PI3K/AKT and ERK signaling pathway in MCL cells. The combination therapy contributed to the inactivation of NF-κB and AKT in MCL cell lines. However, cleaved caspase-3 was up-regulated after combined treatment. Our study showed that PI3K/p110σ is a novel therapeutic target in MCL, and the underlying mechanism could be the blocking of the PI3K/AKT and ERK signaling pathways. These findings provided a basis for clinical evaluation of CAL-101 and a rationale for its application in combination therapy, particularly with BTZ