Objective To investigate the characteristic of diagnosis and treatment of traumatic diaphragm rupture.Methods The characteristic of diagnosis and treatment of 32 cases with traumatic diaphragm rupture was analyzed retrospectively.14 cases were injured by sharp instrument and the other cases with blunt injury mainly caused by traffic accidents.Results Of 32 cases,19 had diaphragmatic ruptures preoperatively,13 diaphragmatic rupture was found during the operation.28 cases cured and 4 cases died.Conclusions The mechanism of traumatic diaphragm rupture and patients' symptoms and sign are severe and complicate with a high shock and mortality.Correct diagnosis and management of traumatic diaphragm rupture are very important.The treatment principle is thoracic injures first and laparotomy second.

Objective To investigate the role of spinal hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in dexmedetomidine-produced antinociceptic effect.Methods In vivo experiment Thirty wild type C57BL/6J mice and 30 HCN1 gene knockout (HCN1-/-) mice, aged 2-3 months, weighing 19-25 g, were randomly divided into 5 groups (n=6 each) using a random number table: control group (group C), and dexmedetomidine 10, 20, 30 and 40 μg/kg groups (Dex10, Dex20,Dex30 and Dex40 groups).In Dex10, Dex20, Dex30 and Dex40 groups, dexmedetomidine 10, 20, 30 and 40 μg/kg were intraperitoneally injected, respectively.The equal volume of normal saline was given in group C.Before dexmedetomidine administration, and at 15, 30, 45, 60, 75, 90, 105 and 120 min after dexmedetomidine administration, tail flick latency to a thermal nociceptive stimulus was measured, and the percentage of the maximum possible effect (MPE％) was calculated.In vitro experiment HCN1 and HCN2 plasmids and green fluorescent plasmids were transfected into HEK293 cells with liposome 2000.At 24-48 h after transfection, HCN1 and HCN2 channel currents were recorded using whole-cell patch clamp technique.HCN channel currents were recorded as baseline value after rupture of membrane.HEK293 cells were perfused with the extracellular fluid containing different concentrations of dexmedetomidine (0.1, 1.0 or 10.0 μmol/L).After the cells were perfused with dexmedetomidine 0.1 μmol/L for 5 min, HCN currents were recorded.The inhibition rate of currents were calculated.After washout, HCN currents were recorded after the cells were perfused with the next concentration for 5 min.The half-maximal activation voltage (V1/2) of HCN channels and the curve slope were recorded.The difference in V1/2 before and after administration (△V1/2) were calculated.Results Compared with group C, MPE％ was significantly increased in Dex10 group-Dex40 group of wild type and HCN1-/-mice (P＜0.05).Compared with Dex30 and Dex40 groups of wild type mice, MPE％ was significantly decreased in Dex30 and Dex40 groups of HCN1-/-mice (P＜0.05).There was no significant difference in MPE％ between Dex10 group and Dex20 group of wild type and HCN1-/-mice (P＞0.05).Compared with the baseline value, the currents and V1/2 of HCN1 and HCN2 channels in HEK293 cells were significantly decreased when the cells were perfused with dexmedetomidine 0.1, 1.0 and 10.0 μmol/L (P＜0.05).Compared with the value when the cells were perfused with dexmedetomidine 0.1 μmol/L, the currents and V1/2 of HCN1 and HCN2 channels in HEK293 cells were significantly decreased, and inhibition rate of currents and △ V1/2were increased when perfused with dexmedetomidine 1.0 and 10.0 μmol/L (P＜0.05).Compared with the value when the cells were perfused with dexmedetomidine 1.0 μmol/L, the currents and V1/2 of HCN1 and HCN2 channels in HEK293 cells were significantly decreased, and inhibition rate of currents and △ V1/2were increased when perfused with dexmedetomidine 10.0 μmol/L (P＜0.05).There was no significant difference in the activation curve slope of HCN1 and HCN2 channel currents in HEK293 cells when the cells were perfused with dexmedetomidine 0.1, 1.0 and 10.0 μmol/L (P＞0.05).Conclusion Dexmedetomidine-produced antinociceptic effect is likely related to the inhibition of spinal HCN channel opening.

French hospital administrators have undergone several changes to meet the needs of economic and social development,resulting in the pattern of hospital administration by both the central government and regional organizations.This paper made descriptions and analysis of the French hospital administrators and came up with the following insights:Making public hospitals as the main health service provider benefits provision of public services; public and private hospitals can jointly meet public service needs under government regulation; the government should focus on controlling health care resources;medical service system needs an overall policy guidance; hospital management organizations should streamline in the reform.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by the destruction of the barrier function of alveolar epithelial cells and capillary endothelial cells and the recruitment of inflammatory cells, which leads to alveolar and interstitial edema, hyaline membrane formation and inflammatory infiltration of the lungs, etc. The mechanism is not completely defined. The current treatment plan focuses on comprehensive treatments such as ventilator support treatment, fluid management, and nutritional support, but the prognosis is still poor. Studies have shown that extracellular vesicle microRNA (miRNA) from different sources participate in regulating the function of epithelial cells, endothelial cells and phagocytes in different ways, thus aggravating or improving ALI, and have diagnostic, differential diagnosis and the therapeutic value. In this article, the mechanism, diagnostic and differerntial value of extracellular vesicle miRNA from different sources in ALI and the therapy of extracellular vesicle miRNA from stem cell in ALI are reviewed.

Objective To investigate whether human RhoA is modified by SUMO. Methods Overlap extension PCR and double digestion technique were used to construct the eukaryotic expression vector pcDNA3-3flag-RhoA, which was identified by sequencing. The plasmid was transfected into HEK293T cells and its expression was detected by Western blotting. Immunofluorescence assay was used to detect whether RhoA is co-localized with SUMO. Co-Immunoprecipitation was used to detect whether RhoA is modified by SUMO. Results The recombinant plasmid pcDNA3-3flag-RhoA was successfully constructed and verified. Western blotting showed that the recombinant plasmid pcDNA3-3flag-RhoA expressed abundant fusion protein in HEK293T cells. Immunofluorescence showed that RhoA was co-localized with SUMO2/3 but not with SUMO1. Co-immunoprecipitation verified that RhoA was modified by SUMO2/3 but not SUMO1. Conclusion Human RhoA is modified by SUMO2/3 and probably participates in the regulation of axon regrowth after nervous system injury.

Objective To investigate whether human RhoA is modified by SUMO. Methods Overlap extension PCR and double digestion technique were used to construct the eukaryotic expression vector pcDNA3-3flag-RhoA, which was identified by sequencing. The plasmid was transfected into HEK293T cells and its expression was detected by Western blotting. Immunofluorescence assay was used to detect whether RhoA is co-localized with SUMO. Co-Immunoprecipitation was used to detect whether RhoA is modified by SUMO. Results The recombinant plasmid pcDNA3-3flag-RhoA was successfully constructed and verified. Western blotting showed that the recombinant plasmid pcDNA3-3flag-RhoA expressed abundant fusion protein in HEK293T cells. Immunofluorescence showed that RhoA was co-localized with SUMO2/3 but not with SUMO1. Co-immunoprecipitation verified that RhoA was modified by SUMO2/3 but not SUMO1. Conclusion Human RhoA is modified by SUMO2/3 and probably participates in the regulation of axon regrowth after nervous system injury.

Objective: To investigate the association between expression of phosphoglycerate kinase 1 (PGK1) in liver cancer tissue and prognosis, as well as its influence on metastasis and invasion of hepatocellular carcinoma (HCC) cells. Methods: Overexpression and downregulated expression of PGK1 in HCC cells were mediated by lentivirus to establish hepatoma cell lines with different expression levels of PGK1. The Transwell chamber invasion assay, wound healing assay, and colony-forming assay were used to investigate the influence of PGK1 on metastasis, invasion, and proliferation of HCC cells. Immunohistochemistry was used to measure the expression of PGK1 in liver cancer tissue samples from 116 patients with hepatocellular carcinoma who underwent radical surgery, and the Kaplan-Meier method and the log-rank test were used to determine the association between PGK1 expression and prognosis of patients with liver cancer. Results: HCCLM3 and MHCC97H HCC cells with high metastatic potential had significantly higher expression of PGK1 than Hep3B and Huh7 HCC cells with low metastatic potential. Downregulation of PGK1 expression significantly inhibited the migration (31.2% ± 2.4% vs 12.0% ± 1.3%, t = 21.57, P < 0.01), invasion (58 ± 11 vs 21 ± 8, t = 4.687, P < 0.05), and colony-forming ability (168.6 ± 15.1 vs 118.4 ± 8.1, t = 6.650, P < 0.05) of MHCC97H cells, while overexpression of PGK1 enhanced the migration (62.8% ± 4.4% vs 83.6% ± 6.1%, t = 20.56, P < 0.01), invasion (80 ± 12 vs 121 ± 15, t = 4.603, P < 0.05), and colony-forming ability (52.3 ± 8.6 vs 84.7 ± 9.0, t = 27.18, P < 0.01) of Hep3B cells. The high PGK1 expression group had significantly shorter median disease-free survival time and mean survival time than the low PGK1 expression group (22.00 ± 8.51 vs not reached, P < 0.05; 46.00 ± 16.87 vs not reached, P < 0.01). Conclusions PGK1 is involved in the regulation of metastasis and invasion of HCC cells and can promote the migration and invasion of HCC cells. Therefore, PGK1 may be an important predictor of prognosis and postoperative recurrence in patients with liver cancer.

Objective　To detect the serum procalcitonin (PCT) levels in young patients with acute cerebral infarction (YACI) and study its relationship with the infarct volume of YACI patients.Methods　According to the volume of cerebral infarction,YACI patients (observation group) who were admitted for the first time were divided into large cerebral infarction group（18 patients）,middle cerebral infarction group (31 patients),and small cerebral infarction group (37 patients).The severity of clinical symptoms was determined using the National Institute of Health Stroke Scale score.In addition,72 healthy young people with brain diffusion weighted imaging examinations within the normal range during the same period were selected as the control group.Serum procalcitonin levels were measured by enzyme-linked immune sorbent assay (ELISA).The relationship among serum procalcitonin,young acute cerebral infarction volume and NIHSS score was analyzed.Results　Serum PCT levels in observation group were significantly higher than those in control group,NIHSS of severe group were significantly higher than those of mild group.The levels of PCT in large infarction group was higher than that in middle infarction group and small infarction group,while the levels of PCT in middle infarction group was higher than that in small infarction group.PCT levels were positively correlated with NIHSS score and infarct volume in the observation group.Conclusion　The levels of serum PCT in YACI patients may be related to the inflammatory reaction of the cerebral artery after cerebral infarction and positively related to the volume of cerebral infarction and NIHSS score.PCT concentration can predict the disease severity of YACI patients,and is of clinical application value.

Objective:In this study, we compared the funding rates of applicants who participated in the expert preliminary counseling with those who did not, to explore the role of the expert preliminary counseling in improving the funding rate of the National Natural Science Fund, so as to provide further reference for the management of scientific research.Methods:Statistical methods was used to analyze relevant data from 2012 to 2019 to compare the approval and funding rate of the applicants that participated in and did not participate in the expert preliminary counseling using.Results:From 2012 to 2019, the proportion of funded applicants in the expert preliminary counselling group was 30.45%, and the overall funding rate was 18.51%. Under the same research basis, the funding rate of the group was 29.91%, which was significantly higher than the group did not participate in the expert preliminary counselling (funding rare: 13.59%, P<0.001). Conclusions:We should pay more attention to and participate actively in the expert preliminary counselling, which can increase the quality of the projects and improve their funding rate significantly.

Mitophagy is the selective degradation of damaged mitochondria, and it is of great significance to maintain the normal quantity and quality of mitochondria to ensure cell homeostasis and survival. Necroptosis is a type of programmed cell necrosis that can be induced by excessive mitophagy. Reactive oxygen species (ROS) are produced mainly by mitochondria and can damage mitochondria. Hyperoxic acute lung injury (HALI) is a serious complication of clinical oxygen therapy, and its pathogenesis is not clear. Existing studies have shown that mitophagy and necroptosis are involved in the occurrence of HALI. There are many mechanisms regulating mitophagy and necroptosis, including tumor necrosis factor-α (TNF-α), E3 ubiquitin protein ligase (PINK1/Parkin) protein pathway encoded by PTEN-induced kinase 1/PARK2 gene, phosphoglycerate mutase 5 (PGAM5), etc. PGAM5 has been proved to be a key factor linking mitophagy and necroptosis. Previous studies of our team found that the mechanism of microRNA-21-5p (miR-21-5p) alleviating HALI was related to its pGAM5-mediated inhibition of mitophagy, but the mechanism of PGAM5-mediated mitophagy and necroptosis remains unclear. Therefore, this paper reviews the targets of PGAM5-mediated mitophagy and necroptosis, in order to find clues of lung protection of pGAM5-mediated mitophagy and necroptosis in HALI, and provide theoretical basis for subsequent basic research.