Postoperative radiotherapy increase the overall survival rate offor breast cancer improves overall survivalpatients, but. Nevertheless, the heart is at risk of radioactive heart damageradiation-induced cardiac injury due to its anatomical location, which is inevitably exposed to radiation during radiotherapy. The heart is considered a "high-risk organ" sensitive to radiation, and its radiation dose should be as low as possible. Previous studies have evaluated the effect of overall heart radiation dose on long-term cardiovascular events, but the. However, new study has found that the average heart dose does not accurately reflect the degree of heart radiation exposure. In recent years, more and morewidespread attention has been paid to subclinical cardiac injury after radiotherapy, aiming at early identification of latent cardiac injury. In addition, the relationship between specific cardiac substructural doses and arrhythmias is unclear. This paper focuses onIn this article, the limitations of average cardiac dose in predicting radioactive heart injuryradiation- induced cardiac injury, the indicators of early identification of the indicators for cardiac injury and the influencing factors of radiation-induced cardiac injury in breast cancer radioactive heart injurywere illustrated, and focuses on the relationship between radiation damage of different cardiac substructures and arrhythmia was evaluated, so asaiming to achieve fine cardiac risk management in breast cancer patients and reduce the non-cancer mortality in breast cancer patients.

Objective: To construct evaluation index system of nursing quality in day operation center and to provide the basis for scientific and objective evaluation of nursing quality in day operation center. Methods: Based on Donabedian quality model as the theoretical framework, the evaluation index system of nursing quality in day operation center was constructed by applying literature research, process tracking, hierarchical analysis and Delphi expert letter. Results: The recovery rate of RR for two rounds of questionnaire was 94.12% and 100.00%. The expert authority coefficient Cr values were 0.816/0.857 respectively. The W value of the coordination coefficient was 0.335/0.381, both of which were statistically significant (P < 0.01). Finally, an evaluation index system of quality of assisted fertility treatment care with 3 dimensions, 12 secondary indicators and 48 items was formed. Yaaph software was used to determine the weight coefficients of primary and secondary indicators, and the consistency test (CR<0.1) was performed, and the variation coefficients of all tertiary items were <0.17. Conclusion The weight distribution of the nursing quality index system in day operation center is reasonable, the index entry is clear, and it is scientific and practical.

ObjectiveTo investigate the efficacy and safety of Shengxiantang in the treatment of early Parkinson's disease with autonomic dysfunction of Qi deficiency pattern. MethodA total of 82 eligible patients were randomized into control group （41 cases） and traditional Chinese medicine （TCM） group （41 cases）. On the basis of standardized treatment of western medicine， TCM group was prescribed Shengxiantang while control group were treated with placebo for 12 consecutive weeks additionally. Scale for Outcomes in Parkinson's Disease-Autonomic （SCOPA-AUT） questionnaire， Unified Parkinson's Disease Rating Scale （UPDRS）， Traditional Chinese Medicine Qi Deficiency Symptom Score of Parkinson's Disease （TCMQDSSPD）， serum levels of glutathione peroxidase （GPx） and superoxide dismutase （SOD）， daily dosage of pramipexole and levodopa and benserazide hydrochloride， and safety index were evaluated both before and after treatment. ResultAfter treatment， the total score of SCOPA-AUT， gastrointestinal score， urinary score， and thermoregulatory score in the control group were higher than those before treatment （P<0.01）， while the above sores in the TCM group were lower than those before treatment （P<0.05， P<0.01）. In addition， the cardiovascular score， pupillomotor score， and sexual score in two groups showed no significant difference from those before treatment. After treatment， the total score of SCOPA-AUT， gastrointestinal score， urinary score， and thermoregulatory score in the TCM group were lower than those in the control group （P<0.05， P<0.01）， and cardiovascular score， pupillomotor score， and sexual score showed no significant difference between two groups. After treatment， the total score of TCMQDSSPD， main symptom scores， and minor symptom scores in the control group had no significant difference from those before treatment. The total score of TCMQDSSPD and minor symptom scores of TCM group were lower than those before treatment （P<0.01）， while the main symptom scores of the TCM group showed no significant difference from those before treatment. After treatment， the UPDRS score， serum GPx and SOD levels， and daily dosage of pramipexole and levodopa and benserazide hydrochloride demonstrated no significant difference from those before treatment in the two groups and between the two groups. No abnormality was found in the safety indexes. ConclusionBased on the standardized treatment of western medicine， Shengxiantang can effectively and safely improve the autonomic symptoms of gastrointestinal system， urinary system， and thermoregulation， as well as the symptoms of Qi deficiency syndrome in early Parkinson's disease with autonomic dysfunction.

OBJECTIVES: To investigate the mechanism of comorbidity between non-alcoholic fatty liver disease (NAFLD) and atherosclerosis (AS) based on metabolomics and network pharmacology. METHODS: Six ApoE^－/－ mice were fed with a high-fat diet for 16 weeks as a comorbid model of NAFLD and AS (model group). Normal diet was given to 6 wildtype C57BL/6J mice (control group). Serum samples were taken from both groups for a non-targeted metabolomics assay to identify differential metabolites. Network pharmacology was applied to explore the possible mechanistic effects of differential metabolites on AS and NAFLD. An in vitro comorbid cell model was constructed using NCTC1469 cells and RAW264.7 macrophage. Cellular lipid accumulation, cell viability, morphology and function of mitochondria were detected with oil red O staining, CCK-8 assay, transmission electron microscopy and JC-1 staining, respectively. RESULTS: A total of 85 differential metabolites associated with comorbidity of NAFLD and AS were identified. The top 20 differential metabolites were subjected to network pharmacology analysis, which showed that the core targets of differential metabolites related to AS and NAFLD were STAT3, EGFR, MAPK14, PPARG, NFKB1, PTGS2, ESR1, PPARA, PTPN1 and SCD. The Kyoto Encyclopedia of Genes and Genomes showed the top 10 signaling pathways were PPAR signaling pathway, AGE-RAGE signaling pathway in diabetic complications, alcoholic liver disease, prolactin signaling pathway, insulin resistance, TNF signaling pathway, hepatitis B, the relax in signaling pathway, IL-17 signaling pathway and NAFLD. Experimental validation showed that lipid metabolism-related genes PPARG, PPARA, PTPN1, and SCD were significantly changed in hepatocyte models, and steatotic hepatocytes affected the expression of macrophage inflammation-related genes STAT3, NFKB1 and PTGS2; steatotic hepatocytes promoted the formation of foam cells and exacerbated the accumulation of lipids in foam cells; the disrupted morphology, impaired function, and increased reactive oxygen species production were observed in steatotic hepatocyte mitochondria, while the formation of foam cells aggravated mitochondrial damage. CONCLUSIONS Abnormal lipid metabolism and inflammatory response are distinctive features of comorbid AS and NAFLD. Hepatocyte steatosis causes mitochondrial damage, which leads to mitochondrial dysfunction, increased reactive oxygen species and activation of macrophage inflammatory response, resulting in the acceleration of AS development.
Animals ; Mice ; Non-alcoholic Fatty Liver Disease/metabolism* ; Cyclooxygenase 2/metabolism* ; PPAR gamma/metabolism* ; Reactive Oxygen Species/metabolism* ; Mice, Inbred C57BL ; Hepatocytes ; Macrophages/metabolism* ; Liver