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Purpose As radiation therapy is widely used for the management of pancreatic cancer, identifying novel targets to improve the radiosensitivity of cancer cells is beneficial. Rosiglitazone, a specific peroxisome proliferator-activated receptor γ (PPARγ) agonist, has an inhibitory effect on various types of cancer cells. The purpose of this paper is to investigate the effect of rosiglitazone on the radiosensitivity of pancreatic cancer cells and the potential mechanism. Materials and Methods PPARγ expression in pancreatic cancer and adjacent tissues was evaluated using immunohistochemistry analysis. The viability, migration and invasion ability of PANC1 and PaTu8988 cells were detected using MTT assay, scratch-wound assay and transwell invasion assay. The effect of rosiglitazone on radiosensitivity of the cells was determined using the clonogenic assay. PANC1 cells were inoculated into BALB/c mice to establish tumors. Microarray was used to investigate changes of genes involved. Results Higher PPARγ expression was demonstrated in pancreatic cancer tissues compared with para-carcinoma tissues. Rosiglitazone inhibited the cell viability and enhanced the radiation-induced anti-migration and anti-invasion effect. Rosiglitazone potentiated the radiosensitivity of pancreatic cancer cells and PANC1 xenografts. Microarray analysis revealed that rosiglitazone plus radiation altered the expression of multiple genes and affected multiple pathways. Conclusion Rosiglitazone enhances the radiosensitivity of human pancreatic cancer cells in vitro and in vivo via complex mechanisms.

Supplemental Material, sj-pdf-1-dos-10.1177_15593258211067060 for Serum Metabolomic Analysis of Radiation-Induced Lung Injury in Rats by Yahui Feng, Yiying Gao, Wenling Tu, Yang Feng, Jianping Cao and Shuyu Zhang in Dose-Response

The combined cooling, heating and power (CCHP) microgrid organically combines the CCHP technology and the microgrid technology that integrates renewable power generation. Considering the energy flow characteristics and energy balance of the co-supply microgrid, this paper proposes a multi-time scale coordinated and optimized scheduling method, aiming at the economic operation of the co-supply microgrid under the grid-connected operation mode. For cold/thermal loads with stable supply and demand, a day-ahead economic dispatch model for cold and thermal energy is established, and the particle swarm algorithm is used to solve the model; for real-time fluctuating electric loads, a heuristic energy dispatch strategy is formulated. The simulation and analysis conducted in an industrial park in the north of China have verified the feasibility and economic efficiency of the strategy.

Zhenyu Wang1 *, Wenhao Shen1 *, Xugang Li,2 Yang Feng,1 Kun Qian,1 Gaoren Wang,3 Yiying Gao,1 Xiaohui Xu,4 Shuyu Zhang,1 Ling Yue,1 Jianping Cao1 1School of Radiation Medicine and Protection (SRMP) of Soochow University, State Key Laboratory of Radiation Medicine and Protection, Suzhou 215123, People’s Republic of China; 2Department of Radiotherapy, Anshan Cancer Hospital, Anshan 114036, People’s Republic of China; 3Nantong Tumor Hospital, Affiliated Tumor Hospital of Nantong University, Nantong 226361, People’s Republic of China; 4Department of General Surgery, The First People’s Hospital of Taicang, Taicang Affiliated Hospital of Soochow University, Suzhou 215400, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jianping Cao; Ling Yue Tel +86-512-65880037Email jpcao@suda.edu.cn; yueling@suda.edu.cnPurpose: As radiation therapy is widely used for the management of pancreatic cancer, identifying novel targets to improve the radiosensitivity of cancer cells is beneficial. Rosiglitazone, a specific peroxisome proliferator-activated receptor γ (PPARγ) agonist, has an inhibitory effect on various types of cancer cells. The purpose of this paper is to investigate the effect of rosiglitazone on the radiosensitivity of pancreatic cancer cells and the potential mechanism.Materials and Methods: PPARγ expression in pancreatic cancer and adjacent tissues was evaluated using immunohistochemistry analysis. The viability, migration and invasion ability of PANC1 and PaTu8988 cells were detected using MTT assay, scratch-wound assay and transwell invasion assay. The effect of rosiglitazone on radiosensitivity of the cells was determined using the clonogenic assay. PANC1 cells were inoculated into BALB/c mice to establish tumors. Microarray was used to investigate changes of genes involved.Results: Higher PPARγ expression was demonstrated in pancreatic cancer tissues compared with para-carcinoma tissues. Rosiglitazone inhibited the cell viability and enhanced the radiation-induced anti-migration and anti-invasion effect. Rosiglitazone potentiated the radiosensitivity of pancreatic cancer cells and PANC1 xenografts. Microarray analysis revealed that rosiglitazone plus radiation altered the expression of multiple genes and affected multiple pathways.Conclusion: Rosiglitazone enhances the radiosensitivity of human pancreatic cancer cells in vitro and in vivo via complex mechanisms.Keywords: ionizing radiation, pancreatic cancer, peroxisome proliferator-activated receptor γ, rosiglitazone, radiosensitivity