Objective:To construct an evaluation index system of internal control medical equipment based on the internal control theory of The Committee of Sponsoring Organizations of the Treadway Commission(COSO)and combined with the current situation of medical equipment internal management in public hospitals,so as to provide reference and suggestions for the evaluation of internal control of medical equipment in public hospitals.Methods:Through literature research and expert consultation,the evaluation index system of internal control of medical equipment was preliminarily determined.Using the Delphi method,15 experts from 1 medical college and 3 tertiary hospitals in Beijing who were engaged in the use and management of medical equipment were selected to conduct two rounds of consultation on the evaluation index system of internal control of medical equipment,and the evaluation indicators were scored and screened.The analytic hierarchy process(AHP)was used to determine the index weights,and the internal control evaluation index system of medical equipment in public hospitals based on COSO was constructed.Results:The coefficient of the two rounds of expert consultation was 100%.The authority degree of consulting experts was 0.867.Finally,the evaluation index system of internal control of medical equipment in tertiary public hospitals was formed,which included 5 first-level indicators,17 second-level indicators and 50 third-level indicators.Conclusion:The evaluation index of internal control of medical equipment in public hospitals based on COSO has high expert enthusiasm,authority and coordination.The evaluation index system includes the unit level and the business level of internal control,with a wide coverage,which makes up for the limitations of traditional internal evaluation of medical equipment,which can make up for the limitations of the internal evaluation of traditional medical equipment,improve the internal control system of medical equipment in public hospitals,and optimize the medical equipment management system.

Objective:To construct an effectiveness evaluation model of internal control of medical equipment in public hospitals based on fuzzy analytic network process(F-ANP),and to improve the level of internal control management of medical equipment in hospitals.Methods:Through literature research and analysis,based on the internal control theory system of The Committee of Sponsoring Organizations of the Treadway Commission(COSO),combined with the characteristics of medical equipment management in public hospitals,the effectiveness evaluation model of internal control of medical equipment in public hospitals was established by F-ANP,which was combining analytic network process(ANP)and fuzzy comprehensive evaluation.An empirical analysis was carried out on the internal control of medical equipment in Beijing Friendship Hospital,Capital Medical University.Results:The index system for model evaluation included 5 first-level indicators of control environment,risk evaluation,control activities,information exchange,and supervision mechanism,17 second-level indicators,and 50 third-level indicators.The model was used to evaluate the effectiveness of internal control of medical equipment in the hospital,its maximum membership value was 0.133 7,and the result was"relatively effective",indicating that the construction and implementation of internal control of medical equipment in the hospital were relatively perfect,while the management of scrapping of medical equipment,cost control and equipment informatization construction still need to be improved.Conclusion:The effectiveness evaluation model of internal control of medical equipment of public hospitals based on F-ANP can provide certain reference value for evaluation of the effectiveness of internal control of medical equipment in public hospitals,which is conducive to standardizing internal control of medical equipment,promoting the fine management of medical equipment and ensuring the safety of medical equipment assets.

Objective:To analyze the clinicopathological characteristics of differentiated early cardia cancer and to evaluate the short-term and long-term efficacy of endoscopic submucosal dissection (ESD).Methods:A total of 329 patients (331 lesions) who underwent ESD at Nanjing Drum Tower Hospital from October 2014 to December 2019 and were pathologically confirmed as differentiated early cardia cancer were included in the study and followed up. The endoscopic and pathological data of patients were reviewed to analyze the clinicopathological characteristics of differentiated early cardia cancer. The short-term (including en bloc resection rate, curative resection rate and incidence of short-term complications) and long-term efficacy (including incidence of metachronous cancer, recurrence and distant metastasis, and overall survival rate) of ESD was evaluated.Results:The ratio of male to female in 329 patients with differentiated early cardia cancer was 4∶1, and their age was 65.69±8.02 years. Tumor diameter of ≤2.0 cm accounted for 65.9% (218/331). Most lesions were located on the posterior wall (50.5%, 167/331), followed by the minor curve (36.3%, 120/331). The endoscopic morphology of 0-Ⅱc type accounted for 49.5% (164/331). There were 69.8% (231/331) lesions confined to the mucosal layer. The en bloc resection rate was 100.0% (329/329), and the curative resection rate was 83.3% (274/329). Short-term complications occurred in 28 patients (8.5%). With a median follow-up time of 39 months, 11 patients (3.3%) developed metachronous cancer, 2 (0.6%) developed distant metastasis, and no recurrence occurred. Seven patients died, and the overall survival rate during the follow-up period was 97.9% (322/329). The survival rate of patients with curative resection and additional surgery was 100.0% (3/3), while that without additional surgery was 99.3% (269/271). The survival rate of patients with non-curative resection and additional surgery was 96.0% (24/25), and that without additional surgery was 86.7% (26/30).Conclusion:Most differentiated early cardia cancers are well-differentiated adenocarcinomas, with less than 2 cm in diameter at the time of diagnosis with a low rate of ulcer and vascular invasion. ESD is safe and effective for the treatment of differentiated early cardia cancer with a high rate of curative resection, fewer intraoperative and postoperative complications, low incidences of metachronous cancer, distant metastasis and recurrence, and a high overall survival rate. However, additional surgical treatment is recommended for patients with non-curative resection.

Genome-wide physical protein-protein interaction(PPI)mapping remains a major chal-lenge for current technologies.Here,we reported a high-efficiency BiFC-seq method,yeast-enhanced green fluorescent protein-based bimolecular fluorescence complementation(yEGFP-BiFC)coupled with next-generation DNA sequencing,for interactome mapping.We first applied yEGFP-BiFC method to systematically investigate an intraviral network of the Ebola virus.Two-thirds(9/14)of known interactions of EBOV were recaptured,and five novel interactions were discovered.Next,we used the BiFC-seq method to map the interactome of the tumor protein p53.We identified 97 interactors of p53,more than three-quarters of which were novel.Furthermore,in a more complex background,we screened potential interactors by pooling two BiFC libraries together and revealed a network of 229 interactions among 205 proteins.These results show that BiFC-seq is a highly sensitive,rapid,and economical method for genome-wide interactome map-ping.

Objective To investigate whether elevated parathyroid hormone (PTH) levels could induce endothelial - to - mesenchymal transition (EndMT) and adipocyte transition in endothelial cells (ECs), and to determine the possible underlying mechanism. Methods (1) A rat model of secondary hyperparathyroidism and chronic kidney disease (CKD) was established. The adiposity in bone marrow was detected by oil red O staining. Immunofluorescence staining was performed to detect the expression and localization of cluster of differentiation 31 (CD31) and fibroblast-specific protein 1 (FSP1). (2) The human umbilical vein ECs were cultured in vitro. Western blotting was performed to detect protein expressions of EndMT-related markers CD31, FSP1 and α-smooth muscle actin (α-SMA) in interference groups with different PTH concentrations (0, 10-11, 10-9, 10-7 mol/L PTH for 48 h) and times (0, 12, 24, 48 h, 10-7 mol/L PTH), as well as the expression of β-catenin in interference groups with different PTH concentrations. The localizations of CD31, FSP1 and β - catenin were observed by cell immunofluorescence. Protein expressions of adipocytes markers peroxisome proliferator - activated receptor-γ (PPAR-γ) and CCAAT/enhancer binding protein-α (C/EBP-α) by Western blotting and the degree of adipogenesis by oil red O staining were detected after transformed ECs were cultured in adipogenic culture medium for one week. Small interfering RNA (siRNA) was performed to silenceβ - catenin expression. ECs were divided into control siRNA group, β - catenin siRNA group, PTH +control siRNA group and PTH+β-catenin siRNA group. Protein expressions of CD31, FSP1 and PPAR-γby Western blotting and the degree of adipogenesis by oil red O staining were determined. Results (1) In vivo, compared with the control, CKD rats had increased adipocytes in bone marrow (P＜0.05), and the co-expression of CD31 and FSP1 in bone marrow ECs. (2) In vitro, PTH significantly inhibited the expression of endothelial marker CD31 and increased the expressions of mesenchymal markers FSP1 and α-SMA in concentration-and time-dependent manners. These indexes in 10-7 mol/L PTH group and 0 mol/L PTH group, in 48 h group and 0 h group showed statistical differences (all P＜0.05). In PTH group ECs with 10-7 mol/L PTH for 48 h showed FSP1 accumulation in the cytoplasm and reduced expressions of CD31, and ECs had higher expressions of PPAR-γ and C/EBP-α as well as the degree of adipogenesis than those in control group (all P＜0.05). Furthermore, PTH enhanced the nuclearβ-catenin protein levels in ECs in concentration-dependent. The expressions of β-catenin in 10-7 mol/L PTH group and 0 mol/L PTH group showed statistical differences (P＜0.05). β - catenin expressed in the cytoplasm in control group, while it enter into the nucleus in PTH group. Compared with those in PTH+control siRNA group, the expressions of CD31 and PPAR-γ as well as the degree of adipogenesis decreased in PTH+β-catenin siRNA group (all P＜0.05), while the expression of FSP1 increased (P＜0.05). Conclusions PTH induces ECs - to - adipocytes transition by the canonical Wnt/β - catenin signaling pathway, which might account for bone loss in CKD. Silenced β - catenin expression can inhibit PTH-induced EndMT and adipogenesis.

Objective To explore the role of the DACT2 gene in the occurrence and development of renal cell carcinoma(RCC).Methods The samples of RCC tissues and corresponding tumor-adjacent tissues after radical operation and normal kidney tissues were collected.The methylation specific PCR (MSP) and real time fluorescence reverse transcriptase-PCR (RT-PCR) methods were adopted to detect the methylation status and mRNA expression of DACT2.The streptavidin-peroxidase (SP) method labeled by immunohistochemistry peroxidase was used to examine the expression of β-catenin protein.Then the relationship between DACT2 gene methylation status and mRNA expression with the clinicopathologic characteristics was analyzed.The relationship between DACT2 gene methylation with mRNA and β-catenin expression was analysed,as well.Results The DACT2 mRNA relative expression level in RCC tissues was 0.427±0.025,which was significantly lower than (0.801±0.047) in tumor-adjacent tissues and (0.872±0.022) in normal tissue,the positive rate of DACT2 gene methylation in RCC tissues was 45.76%,which was significantly higher than 6.78% in tumor-adjacent tissues and 5.08% in normal tissues,the difference was statistically significant (P<0.05),while the difference between tumor-adjacent tissues and normal tissues had no statistical significance (P>0.05).The DACT2 gene mRNA expression level in RCC tissues and promoter area methylation occurrence rate had no obvious correlation with the clinical data such as patients age,gender,tumor size,clinical stage and Fuhrman grade (P>0.05).The DACT2 gene mRNA relative level in the methylation group was lower than that in the non-methylation group,the difference was statistically significant (P<0.05).The expression rate of β-catenin protein in cytoplasma in RCC tissues was higher than that in the tumor-adjacent tissues and normal tissues,the difference was statistically significant (P<0.05),moreover,DACT2 gen methylation had a positive correlation with β-catenin protein expression (r=0.324,P=0.012).Conclusion The decrease of DACT2 gene promoter area methylation and mRNA relative expression level may participate in the RCC occurrence,but has no relationship with RCC clinical progression.Methylation occurred in DACT2 gene promoter area may be one of reasons causing mRNA relative expression decrase.DACT2 gene methylation occurrence in RCC tissue might be related to the high expression of β-catenin.

Objective To detect the methylation of Wif-1 gene promoter and its mRNA expression level in renal cell carcinoma, and to explore its possible mechanisms in the development of renal cell carcinoma.Methods The methylation-specific polymerase chain reaction (MSP) and reverse transcription-polymerase chain reaction (RT-PCR) were applied to investigate the methylation status of Wif-1 gene promoter and its mRNA expression levels in renal cell carcinoma (RCC) and normal kidney tissue.Results The percentage of methylation of Wif-1 gene in RCC tissue was significantly higher than that in the corresponding normal kidney tissue (P<0.05).The relative expression quantity of Wif-1 mRNA in RCC tissue was significantly lower than that in corresponding normal kidney tissue (P<0.05).In the RCC tissue, the relative expression of mRNA in the Wif-1 methylation positive group showed no significant difference with that in the methylation negative group.Conclusion Hypermethylation of the Wif-1 promtor in RCC is a frequent phenomenon.

Objective To detect the methylation of Wif-1 gene promoter and its mRNA expression level in renal cell carcinoma, and to explore its possible mechanisms in the development of renal cell carcinoma.Methods The methylation-specific polymerase chain reaction (MSP) and reverse transcription-polymerase chain reaction (RT-PCR) were applied to investigate the methylation status of Wif-1 gene promoter and its mRNA expression levels in renal cell carcinoma (RCC) and normal kidney tissue.Results The percentage of methylation of Wif-1 gene in RCC tissue was significantly higher than that in the corresponding normal kidney tissue (P<0.05).The relative expression quantity of Wif-1 mRNA in RCC tissue was significantly lower than that in corresponding normal kidney tissue (P<0.05).In the RCC tissue, the relative expression of mRNA in the Wif-1 methylation positive group showed no significant difference with that in the methylation negative group.Conclusion Hypermethylation of the Wif-1 promtor in RCC is a frequent phenomenon.

Objective: To investigate the effects of hinokitiol on the proliferative inhibition and apoptosis induction in human clear cell renal cancer 786-O cells. Methods:CCK-8 assays were performed to analyze the effects of hinokitiol on the proliferation of 786-O cells. The apoptosis rate was determined by flow cytometry. EGFP-LC3 microscopy assays were performed to assess the autoph-agy flux. Cleaved Caspase-3, LC3, and P62 were detected by Western blot. Results: Hinokitiol could inhibit the proliferation of the 786-O cells and could induce cell apoptosis via Caspase pathway. Hinokitiol induced the autophagy of 786-O cells, increased LC3 ex-pression, and downregulated P62 expression. Conclusion: Hinokitiol can inhibit the proliferation of 786-O cells and can induce cell apoptosis via autophagy induction.

Background and purpose:MicroRNA (miRNA, miR) plays an important regulatory role in cancer. miR-222 is reported to be up-regulated in various tumors, but its role in renal cell carcinoma (RCC) remains unclear. In this study, we detected the expression of miR-222 in both RCC and adjacent tissue samples. The aim of this study was to investigate the role of miR-222 in RCC. Methods:The expression levels of miR-222 in RCC tissue samples were quantified by quantitative real-time polymerase chain reaction (qRT-PCR). DDIT4 and LC3-Ⅱ protein expressions were determined by Western blot. Dual luciferase assay was performed to verify the target of miR-222. EGFP-LC3 microscopy assay was performed to assess autophagy. Results:Results from qRT-PCR showed that the expression of miR-222 was up-regulated in RCC tissues. Knockdown of miR-222 with speciifc antagomiR decreased the cell viability of 786-O cells, whereas overexpression of miR-222 increased the cell viability (P<0.01). The levels of DDIT4 were up-regulated in 786-O cells transfected with miR-222 antagomiR, whereas overexpression of miR-222 induced the down-regulation of DDIT4 expression. Data from dual luciferase assay indicated that miR-222 directly targeted the expression of DDIT4. Consistently, the expression of DDIT4 in RCC tissues was down-regulated compared with adjacent tissues. Knockdown of miR-222 in 786-O cells induced a signiifcant increase of autophagosome formation and LC3 lipidation.These results supported that miR-222 could inhibit autophagy in RCC cells, which may affect the clinical characteristcs of RCC. Conclusion: miR-222 is up-regulated in RCC and can inhibit the autophagy of RCC cells through down-regulating the expression of DDIT4.