Chongxiao Qu

Area of research

Genetics · Molecular Biology

Research interest

Research topics from publications: A Model of Metabolic Syndrome and Related Diseases with Intestinal Endotoxemia in Rats Fed a High Fat and High Sucrose Diet; Long non-coding RNA ATXN8OS promotes ferroptosis and inhibits the temozolomide-resistance of gliomas through the ADAR/GLS2 pathway; Glycine protects against high sucrose and high fat-induced non-alcoholic steatohepatitis in rats; Targeted Knockdown of IQGAP1 Inhibits the Progression of Esophageal Squamous Cell Carcinoma In Vitro and In Vivo; Assessment of tumor-associated immune cells in laryngeal squamous cell carcinoma; Conventional MR and DW imaging findings of cerebellar primary CNS lymphoma: comparison with high-grade glioma; Diffusion kurtosis imaging combined with dynamic susceptibility contrast-enhanced MRI in differentiating high-grade glioma recurrence from pseudoprogression; Elevated Expression of NOTCH1 Associates with Lymph Node Metastasis of Gastric Cancer and Knock-Down of NOTCH1 Attenuates Tumor Cell Progression; Clinical significance and correlation of miR-200c and P-gp expression in gastric cancer and the effects on multidrug resistance; Characteristics of the isocitrate dehydrogenase gene and telomerase reverse transcriptase promoter mutations in gliomas in Chinese patients. Representative work: AIM: We sought develop and characterize a diet-induced model of metabolic syndrome and its related diseases. METHODS: The experimental animals (Spague-Dawley rats) were randomly divided into two groups, and each group was fed a different feed for 48 weeks as follows: 1) standard control diet (SC), and 2) a high sucrose and high fat diet (HSHF). The blood, small intestine, liver, pancreas, and adipose tissues were sampled for analysis and characterization. RESULTS: Typical metabolic syndrome (MS), non-alcoholic fatty liver disease (NAFLD), and type II diabetes (T2DM) were common in the HSHF group after a 48 week feeding period. The rats fed HSHF exhibited signs of obesity, dyslipidemia, hyper // Xin Zhou 1 , Dewu Han 1 , Ruiling Xu 1 , Huiwen Wu 1,2 , Chongxiao Qu 3 , Feng Wang 1 , Xiangyu Wang 4 and Yuanchang Zhao 1 1 Department of Pathophysiology, Basic Medical Science, Shanxi Medical University, Taiyuan, Shanxi, China 2 Science & technology center of Fenyang College, Shanxi Medical University, Fenyang, Shanxi, China 3 Department of Pathology, Shanxi Provincial People’s Hospital, Taiyuan, S

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