Objective To compare the safety,effectiveness and affordability of robotic-assisted thoracic surgery and video-assisted thoracic surgery in the treatment of malignant pulmonary tumors,and provide ref-erences for the management of selection of different surgical strategies for malignant pulmonary tumors in hospitals and medical insurance departments.Methods The medical records homepages and information sys-tem data of patients with malignant pulmonary tumors who underwent major thoracic surgery in this hospital and discharged from January 1 to December 31,2022 were obtained.The patients were divided into the robotic-assistedthoracic surgery group and video-assisted thoracic surgery group according to the surgical methodolo-gies.After performing propensity score matching (PSM),no statistically significant difference was observed in baseline data between the two groups (117 cases in each group).Then the indicators of safety,effectiveness and affordability were compared between the two groups.Results Concerning the safety,the postoperative in-cision infection rate in the robotic-assisted thoracic surgery group was significantly lower than that in the vide-o-assisted thoracic surgery group (P<0.05),and the amount of intraoperative blood loss and postoperative complication rate were not significantly different between the two groups (P>0.05).Regarding the effective-ness,the average surgical duration in the robotic-assisted thoracic surgery group was appreciably shorter than that in the video-assisted thoracic surgery group (P<0.05),no patient in the two groups was converted to open thoracotomy,and there was no statistically significant difference in the average length of hospital stay and postoperative hospital stay between the two groups (P>0.05).With regard to the affordability,the aver-age inpatient expenditure per case and average daily inpatient expenditure per case in the robotic-assisted tho-racic surgery group were significantly higher than those in the video-assisted thoracic surgery group (P<0.05),and there were disparities in the cost structure between the two procedures.The medical cost,adminis-tration cost and consumables cost in the robotic-assisted thoracic surgery group were significantly higher than those in the video-assisted thoracic surgery group (P<0.05).The cost of medical technology in the robotic-assisted thoracic surgery group was significantly lower than that in the video-assisted thoracic surgery group (P<0.05).Conclusion Physicians should comprehensively consider the clinical efficacy and cost burden of patients when selecting the robotic-assisted thoracic surgery or the video-assisted thoracic surgery,and the monitoring and evaluation of the utilization of clinical robotic-assisted thoracic surgery should be strength-ened.

OBJECTIVE To analyze the grouping effect and composition of hospitalization costs for cases of patients with malignant proliferative disease under the diagnosis-related group （DRG） payment system， as well as any changes， in order to provide a basis for medical institutions to improve DRG payment-related measures， control drug costs， and for relevant departments to make decisions. METHODS The data of patients with malignant proliferative disease cases were collected from a “Third Grade Class A” hospital in 2021 and 2022， and the variation coefficient （CV） was used to evaluate the grouping of DRG. The structural variation degree and the new grey correlation analysis were used to study the structural variation of hospitalization cost and the correlation degree between the hospitalization cost and the cost of other items. RESULTS The overall reduction in variance （RIV） for the DRG group of patients with malignant proliferative disease was 79.36%； the CV of other groups were all lower than one except that the RW21 group was 1.09. Compared with 2021， the hospitalization cost for patients with malignant proliferative disease in 2022 decreased by 17.80%， and the decreases in management fees and drug costs were 32.15% and 21.30%， respectively， while the per capita medical expenses increased by 17.26%. The new grey correlation degree of drug cost decreased， but that of medical expenses increased. CONCLUSIONS Under the DRG payment system， hospitalization costs for patients with malignant proliferative disease in the sample hospital decrease， but the grouping efficiency of RW21 and other disease groups needs improvement， and the cost structure needs optimization.

Abstract OBJECTIVE To explore the material basis and mechanism of Crataegi Fructus in improving metabolic hypertension(MH) by using network pharmacology and molecular docking technique.METHODS The components of Crataegi Fructus were collected by HERB, ETCM database and literature survey; screening all ingredients of Crataegi Fructus to improve MH targets through databases such as SwissTargetPrediction and GeneCards; build "active ingredient-target-disease" network of Crataegi Fructus with Cytoscape software; DAVID was used to analyze GO enrichment and KEGG pathway. The core components and core targets were verified by molecular docking with Autodock software. RESULTS The total of 89 active components were screened from Crataegi Fructus and acted on 84 targets. Among them, the core active components of Crataegi Fructus to improve MH were maslinic acid, fomefficinic acid B, linolenic acid, linoleic acid, methyl-n-nonylketone, apigenin, ursolic acid, etc. The core targets were CYP19A1, PPARA, ESR1, PTGS2, PPARG, NR3C1, MMP9, TNF, etc. The mechanism of action mainly involved multiple signaling pathways such as inflammation, glycolipid metabolism, and vascular endothelial function. Molecular docking showed that the core active ingredients of Crataegi Fructus had high affinity with core targets. CONCLUSION Crataegi Fructus may regulate multiple signaling pathways such as TNF, IL-17, AGE-RAGE, HIF-1, cGMP-PKG through multi-component regulation, thereby inhibiting inflammatory response, improving glucose and lipid metabolism abnormalities, and improving vascular endothelial function, so as to comprehensively exert the role of improving MH in various aspects.

OBJECTIVE：To provide reference for improving medical insurance reimbursement for multi-indication drugs based on value-based pricing in China. METHODS：The theory and practice of value-based pricing for multi-indication drugs were sorted out，and the value standards and medical insurance reimbursement strategies based on value-based pricing in France，Germany，UK，Italy and Sweden were analyzed，so as to provide the suggestions for medical insurance reimbursement of multi-indication drugs in China. RESULTS & CONCLUSIONS：The realization of value-based pricing first needed to develop a value framework to define，measure and integrate value，and then established a model to convert the total value into price. The overall idea of value-based pricing for multi-indication drugs was consistent，but there were differences in the value standard. In the UK and Sweden， quality-adjusted life years （QALYs） and incremental cost-effectiveness ratios （ICERs） measured by pharmacoeconomicsare used as the value standard. France，Germany and Italy were more focused on the therapeutic value and clinical benefit improvement. As for medical insurance reimbursement strategies，France adopted single weighting method based on expected volume. Germany adopted combination weighting method based on value and volume. UK introduced the Patient Access Schemes and Italy introduced the Managed Entry reements，both based on the nominal reimbursement standard. Sweden adopted independent reimbursement for different indications by different brand names. It is suggested that China can explore the value-based pricing strategies of multi-indication drugs on the basis of the above international experiences，reference and use these variety of medical insurance reimbursement strategies comprehensively. Simultaneously，the information collection mechanism of patients and drug use should be improved to provide data support for the implementation of China’s value-based pricing and reimbursement strategies for multi-indication drugs.

Lymphoma is one of the most common malignant tumor of the hematologic system. The genome instability is not only an important molecular basis for the development of lymphoma, but also has important value in the diagnosis and prognosis of lymphoma. There are 2 types of genome instability: Microsatellite instability (MSI/MIN) at gene level and chromosomal instability at chromosome level. Through the study on genes associated with lymphoma, the unstable genes associated with lymphoma could be found, meanwhile the mechanism of its occurrence and development of lymphoma could be explored, and the important basis of molecular biology could also be provided in the field of current hot lymphoma precision medical research.
Genomic Instability ; Humans ; Lymphoma/genetics* ; Microsatellite Instability ; Microsatellite Repeats ; Neoplasms

OBJECTIVE: To explore the effect of the oxidored nitro domain containing protein 1 (NOR1) gene knockdown on the biological behavior of HeLa cells in cervical carcinoma. METHODS: The recombinant plasmids pSUPER-shNOR1-1, pSUPER-shNOR1-2 and pSUPERscramble, which targeted to NOR1 gene, were constructed by pSUPER.neo+GFP vector, transfected into HeLa cells respectively using Lipofectamine 2000 reagent, and followed by G418 selection. The expression level of NOR1 mRNA and protein were determined by RT-PCR and Western blotting, respectively. Methyl thiazolyl tetrazolium (MTT) assay was performed to determine the growth curve of cell viability. The stable transfectants were treated with H₂O₂ and cell apoptosis was determined by Hoechst 33258 staining and terminal deoxynucleotidyl transferasemediated dUTP nick end labeling (TUNEL) assay. The expression levels of Bcl-2, cleaved caspase 9 and poly ADP-ribose polymerase (PARP) were measured by Western blot. RESULTS: NOR1- knockdown HeLa cells were successfully constructed by transfection of pSUPER-shNOR1-1 or pSUPER-shNOR1-2 plasmids into HeLa cells. MTT assay showed that the silence of endogenous NOR1 in HeLa cells could lead to the increase in cell viability and proliferation, and the inhibition of H₂O₂-induced apoptosis compared with the negative control. Western blot showed that the expression level of active caspase 9 and cleaved PARP was inhibited in NOR1-knockdown cells when they were treated with H₂O₂ while the expression level of Bcl-2 protein increased. CONCLUSION Silence of endogenous NOR1 facilitates the cell viability and growth of HeLa cells, and attenuates HeLa cells apoptosis induced by H₂O₂, which might be mediated by up-regulation of Bcl-2 level and down-regulation of the cleaved caspase 9 cascade.
Apoptosis ; Caspase 9 ; metabolism ; Cell Survival ; Down-Regulation ; Gene Knockdown Techniques ; Genetic Vectors ; HeLa Cells ; Humans ; Hydrogen Peroxide ; Membrane Transport Proteins ; genetics ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; RNA, Messenger ; Transfection ; Up-Regulation

Despite seminal studies in the 1920s by Warburg showing a characteristic metabolic pattern for tumors, cancer bioenergetics has otfen been relegated to the backwaters of cancer biology. Recent studies have shown that metabolism in the tumor tissue is far more complicated than we previously knew. Despite vigorous glycolysis, in fact, the tumor tissue still retains mitochondrial aerobic metabolism. Mitochondria is one of the main sites of the biosynthesis process of tumor cells. Recent studies revealed that abnormal fatty acid metabolism. Amino acid metabolism plays a key role in the tumorigenesis. The metabolic network in tumor cells was reprogrammed, leading to nutrition lfux reorganization and re-direction. Metabolism reprogramming in tumor cells facilitates the balance between the needs of energy supply and the synthesis of biological macromolecules. Targeting cell metabolism is not intended to interfere the energy supply of tumor cells but to affect the synthesis of metabolic rate, thereby inhibiting the proliferation of the tumor. hTe review focuses on the importance of metabolic reprogramming in tumor development and cancer therapy. We summarize what is currently known about metabolic reprogramming and establish a framework to understanding its contribution to the altered metabolism of cancer cells.

The link between nonresolving inflammation and cancer is well documented. On the one hand, epidemiologic evidence supports that approximately 25% of all human cancer worldwide is caused by nonresolving inflammation. On the other hand, inflammatory cells are found in the microenvironment of most, if not all, tumors. In the tumor micro-environment, inflammatory cells and molecules influence almost every aspect of cancer. MicroRNAs (miRNAs) participate in the initiation and progression of nonresolving inflammation-related cancer by regulating the key genes and related signaling pathways. Further investigation into the molecular mechanisms by which miRNAs carry out their functions will be of great value in the prevention, early diagnosis, and treatment of tumors.
Chronic Disease ; Humans ; Inflammation ; complications ; genetics ; immunology ; Inflammation Mediators ; immunology ; MicroRNAs ; genetics ; Neoplasms ; etiology ; genetics ; Tumor Microenvironment

OBJECTIVE: To analyze the effect of DNA hypermethylation on NOR1 promoter activity and expression. METHODS: NOR1 promoter plasmids were treated with SssI methyltransferase. The plasmids were modified by sodium bisulfite and purified. Sodium bisulfite-modified plasmids were subjected to PCR with primers designed to analyze the methylation status of 26 CpG sites in a 311-bp region of the NOR1 promoter. Cells were transfected by methylated or mock-methylated promoter plasmids. The promoter activities were assessed by the luciferase levels of cell lysates or by directly observing GFP expression under fluorescence microscope. HL60 cells were treated with different concentrations of 5-aza-dC. Total RNA was isolated from harvested cells. Real-time RT-PCR was used to measure the expression level of NOR1 mRNA. RESULTS: Bisulfite sequencing confirmed that SssI methyltransferase treatment successfully resulted in intensive hypermethylation of the NOR1 promoter plasmids. The promoter activity of NOR1 promoter plasmids was totally blocked by SssI methyltransferase treatment. NOR1 expression levels in HL60 cells were restored by 5-aza-dC treatment. CONCLUSION NOR1 promoter plasmids are intensively hypermethylated by SssI methyltransferase treatment. The promoter activity of NOR1 promoter plasmids are totally blocked by SssI methyltransferase treatment. The 5-aza-dC treatment may restore the endogenous NOR1 mRNA level in HL60 cells.
Azacitidine ; analogs & derivatives ; pharmacology ; Base Sequence ; Cell Line, Tumor ; CpG Islands ; DNA Methylation ; DNA Modification Methylases ; antagonists & inhibitors ; DNA-Cytosine Methylases ; pharmacology ; Decitabine ; Epigenesis, Genetic ; Gene Silencing ; HL-60 Cells ; Humans ; Membrane Transport Proteins ; genetics ; metabolism ; Molecular Sequence Data ; Nasopharyngeal Neoplasms ; pathology ; Promoter Regions, Genetic ; genetics ; RNA, Messenger ; genetics ; metabolism

Objective To investigate the function and mechanism of miR-149 in nasopharyngeal carcinoma (NPC).Methods The expression of miR-149 was examined by real-time PCR and calculated by 2-△△Ct method. The cell proliferation was analyzed by MTT assay. The cell migration and invasion were shown by the wound healing assay and transwell migration assay, and the expression of E-cadherin was detected by Western blot. Results The expression of miR-149 was higher in NPC cell lines 5-8F and 6-10B than that in normal immortalized nasopharyngeal epithelial NP69. MTT assay showed that miR-149 promoted the proliferation of NPC cell lines. The wound healing assay showed miR-149 promoted the mobility and invasion of NPC cell lines. Inhibition of miR-149 reduced the ability of NPC cell lines to proliferate and invade. miR-149 downregulated the expression of E-cadherin, whereas antagomir which mediated knockdown of miR-149 significantly upregulated the expression of E-cadherin. Conclusion miR-149 might be involved in the invasion and metastasis of NPC through regulation of epithelial-mesenchymal transition (EMT).