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        Structure and magnetic properties of Ni0.5Zn0.5Mn0.5-xMoxFe1.5O4 ferrites prepared by sol-gel auto-combustion method

        Jiajia Pei,Zhi Wang,Yu Gao,Haoming Zhang 한국물리학회 2019 Current Applied Physics Vol.19 No.4

        A series of Mo doped Ni-Mn-Zn ferrites compounds with the formula Ni0.5Zn0.5Mn0.5-xMoxFe1.5O4 (x=0, 0.025, 0.05, 0.075 and 0.1) were first synthesized by sol-gel auto-combustion method. The X-ray diffraction (XRD), field emission scanning electron microscopy (FESEM), Fourier transform infrared spectroscopy (FTIR), and vibrating sample magnetometer (VSM) analysis were carried out to characterize the microstructural and magnetic properties of ferrites. Rietveld refinement of X-ray diffraction data confirmed the formation of cubic spinel structure and the emergence of FeMoO4 phase with the substitution of Mo6+ contents. The grain size increased remarkably due to the formation of the liquid phase. The saturation magnetization (Ms) increased while the coercivity (Hc) decreased from 67.3 to 12.1 Oe due to the decrease of magneto-crystalline anisotropy constant. The initial permeability (μi) increased significantly from 34 (x=0) to 114 (x=0.075) and later decreased for x=0.1. In our experiment, Ni0.5Zn0.5Mn0.425Mo0.075Fe1.5O4 ferrite presented the best microstructure and soft magnetic properties.

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        PROM2 promotes gemcitabine chemoresistance via activating the Akt signaling pathway in pancreatic cancer

        Wenbin Li,Yue Zhu,Kelin Zhang,Xianhuan Yu,Haoming Lin,Wenrui Wu,Yaorong Peng,Jian Sun 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

        In recent years, the deoxycytidine analogue gemcitabine (2′,2′,-difluorodeoxycytidine) has become the first-line chemotherapeutic agent for patients with pancreatic cancer. However, due to the intrinsic resistance of pancreatic cancer cells, gemcitabine-based chemotherapy yields limited disease control, with >85% disease progression at 6 months from diagnosis. Therefore, elucidating the mechanisms of chemoresistance is a critical step in improving cancer therapy, especially for the treatment of pancreatic cancer. We show PROM2, a transmembrane glycoprotein, is ubiquitously upregulated in pancreatic cancer cell. We also found higher PROM2 expression is associated with shortened overall and disease-free survival times in patients diagnosed with pancreatic cancer. We provide evidence that PROM2 promotes chemoresistance to gemcitabine both in vivo and in vitro. Mechanistically, we demonstrate that PROM2 could directly interacted with Akt and activates the Akt signaling pathway, which thus inhibiting gemcitabineinduced apoptosis. As further evidence, we show PROM2 expression and Akt phosphorylation both promote gemcitabine chemoresistance, and cause poorer survival in clinical samples with pancreatic cancer. Combining gemcitabine with the Akt inhibitor MK-2206 facilitated significant tumor shrinkage and dramatically elevated the survival status in mice xenografted with pancreatic cancer cells. Our findings not only establish PROM2 as a novel positive regulator of the Akt signaling pathway and a candidate prognostic indicator of gemcitabine response, but also provide a neo-therapeutic approach for patients resistant to gemcitabine treatment.

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