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- 저자 : Haoming Zhang (검색결과 3 건)
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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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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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The effect of canagliflozin on gut microbiota and metabolites in type 2 diabetic mice
Zeng Li,Ma Jideng,Wei Tiantian,Wang Hao,Yang Guitao,Han Chongxiang,Zhu Tao,Tian Haoming,Zhang Min 한국유전학회 2024 Genes & Genomics Vol.46 No.5
Background Sodium glucose cotransporter 2 inhibitor (SGLT2i) represent a new type of hypoglycemic medicine that can cause massive loss of glucose from the urine, which have several benefits of reducing body weight and improving the prognosis of cardiovascular and kidney diseases. Although they are oral medicated hypoglycemic agents, their effects on the gut microbiome and function have been unclear. Objective In order to describe the effects of canagliflozin on intestinal flora and metabolites, diabetic mice were randomized to receive canagliflozin or isoconcentration carboxymethylcellulose sodium by gavage for 8 weeks. Feces were collected for 16 S rRNA gene and LC-MS/MS analysis and enriched metabolic pathways through Kyoto Encyclopedia of Genes and Genomes (KEGG). Liver, muscle, intestinal, fat were collected for qRT-PCR according to KEGG enriched metabolic pathways. Results Our results showed that canagliflozin significantly increased GLP-1 level and impacted on the composition of gut microbiota and metabolites. It mainly increased Muribaculum, Ruminococcaceae_UCG_014, Lachnospiraceae-UCG-001, decreased ursodeoxycholic acids (UDCA) and hyodeoxycholic acids (HDCA), and increased fatty acids metabolites in feces. Conclusion In conclusion, we analyzed the changes of intestinal microbial composition and metabolites in diabetic mice after canagliflozin intervention and found that canagliflozin influenced intestinal fatty acid and bile acid (BA) metabolism. This study will provide reference for subsequent SGLT2i and intestinal related research. Background Sodium glucose cotransporter 2 inhibitor (SGLT2i) represent a new type of hypoglycemic medicine that can cause massive loss of glucose from the urine, which have several benefits of reducing body weight and improving the prognosis of cardiovascular and kidney diseases. Although they are oral medicated hypoglycemic agents, their effects on the gut microbiome and function have been unclear. Objective In order to describe the effects of canagliflozin on intestinal flora and metabolites, diabetic mice were randomized to receive canagliflozin or isoconcentration carboxymethylcellulose sodium by gavage for 8 weeks. Feces were collected for 16 S rRNA gene and LC-MS/MS analysis and enriched metabolic pathways through Kyoto Encyclopedia of Genes and Genomes (KEGG). Liver, muscle, intestinal, fat were collected for qRT-PCR according to KEGG enriched metabolic pathways. Results Our results showed that canagliflozin significantly increased GLP-1 level and impacted on the composition of gut microbiota and metabolites. It mainly increased Muribaculum, Ruminococcaceae_UCG_014, Lachnospiraceae-UCG-001, decreased ursodeoxycholic acids (UDCA) and hyodeoxycholic acids (HDCA), and increased fatty acids metabolites in feces. Conclusion In conclusion, we analyzed the changes of intestinal microbial composition and metabolites in diabetic mice after canagliflozin intervention and found that canagliflozin influenced intestinal fatty acid and bile acid (BA) metabolism. This study will provide reference for subsequent SGLT2i and intestinal related research.
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