Price management plays an important role in implementing government price policies,reducing health care costs and improving economic efficiency in the hospital.The article discusses the ways to improve hospital' s price management,and to improve economic efficiency from the following four aspects.First,to step up publicity,foster the awareness of price management,and improve the staff awareness of price management.Second,in the event of introducing new services and technologies,to timely establish reasonable and legal charging standards,and introduce business opportunities for the hospital.Third,to strengthen price management information system,improving the accuracy of charging.Fourth,to strengthen cost accounting for the purposes of lower expenses and higher efficiency,and reducing patients' financial burden.

Identifying the importance of improving pricing control in military hospitals based on a review of the status quo of such management.In addition to an analysis of difficulties in pricing control in these hospitals,proposing to build an efficient pricing control system with a better understanding of the significance of pricing control.Establishing rules and regulations on medical charges to regulate pricing;making use of computer networks in the management for medical charges transparency;enhancing charges securitization to rule out excessive charges;improving general competence of pricing workers to regulate pricing control,All these five measures will help enhance pricing control in military hospitals.

At present, the development of hospital in transition period the doctor-patient contradiction, mutu-al trust foundation weak such outstanding contradictions and problems, based on the analysis of facing the outpatient service charge first overall service consciousness; Contradiction link concentration; Hospital information system support does not reach the designated position; Charge personnel are not familiar with services such as business management status, on the basis of train first service consciousness concrete measures are put forward. Namely:strengthen the psychological counseling, advocate humanistic care;carry out training assessment, improve human-istic quality;strengthen the construction of standardization, the standard outpatient service charging process;develop information platform, optimize charging way;strengthen the department cooperation, build a system integration work.

Objective:To explore the effects of K-ras gene on the expressions of oncogenes and cancer suppressor genes in human bronchial epithelial (HBE) cells which were exposed to PM 2.5. Methods:According to the mRNA sequence of K-ras gene provided by GenBank in September 2019, interference sequences were designed and synthesized, and the recombinant lentiviral vector was transfected into HBE cell to construct the K-ras gene-silenced cells. HBE cells and K-ras gene-silenced cells were exposed to 10 μg/ml, 50 μg/ml PM 2.5 suspension and 10 μmol/L Cr 6+. Real-time fluorescent quantitative PCR was used to detect the mRNA expression levels of c-myc, c-fos, N-ras, cyclin-D1, p16 and p53 genes, the expression levels of p53 and c-myc proteins were detected by Western blot. Results:In K-ras silenced cell group, K-ras mRNA expression level decreased (80.5%±3.6%) and K-ras protein level decreased (58.9%±4.7%) when compared with the control group ( P<0.01) . Compared with the correspoding cell control group without exposure, the mRNA expression levels of c-myc, c-fos, N-ras and cyclin-D1 genes in HBE cell group exposed to different concentrations of PM 2.5, K-ras silenced cell group exposed to different concentrations of PM 2.5, HBE cell group exposed to 10 μmol/L Cr 6+ and K-ras silenced cell group exposed to 10 μmol/L Cr 6+ were increased, the mRNA expressions of p16 and p53 genes were decreased ( P<0.01) . Compared with HBE cell group exposed to 10 μg/ml PM 2.5, the mRNA expressions of c-myc, c-fos and p16 genes in K-ras silenced cells exposed to 10 μg/ml PM 2.5 were decreased, and the p53 mRNA level was increased ( P<0.01) . Compared with HBE cell group exposed to 50 μg/ml PM 2.5, the mRNA expression levels of c-fos, N-ras, cyclin-D1, p16 and p53 genes in K-ras silenced cell group exposed to 50 μg/ml PM 2.5 were decreased ( P<0.01) . Compared with the HBE cell group without exposure, c-myc protein increased and p53 protein decreased in HBE cells exposed to 50 μg/ml PM 2.5 ( P<0.05) . Compared with the K-ras silenced cell group without exposure, c-myc protein increased in K-ras silenced cells exposed to 50 μg/ml PM 2.5 ( P<0.05) . Conclusion:PM 2.5 can increase the expression levels of oncogenes in HBE cells, and K-ras gene silencing can inhibit the expression levels of oncogenes in HBE cells treated with PM 2.5.

Objective:To explore the effects of K-ras gene on the expressions of oncogenes and cancer suppressor genes in human bronchial epithelial (HBE) cells which were exposed to PM 2.5. Methods:According to the mRNA sequence of K-ras gene provided by GenBank in September 2019, interference sequences were designed and synthesized, and the recombinant lentiviral vector was transfected into HBE cell to construct the K-ras gene-silenced cells. HBE cells and K-ras gene-silenced cells were exposed to 10 μg/ml, 50 μg/ml PM 2.5 suspension and 10 μmol/L Cr 6+. Real-time fluorescent quantitative PCR was used to detect the mRNA expression levels of c-myc, c-fos, N-ras, cyclin-D1, p16 and p53 genes, the expression levels of p53 and c-myc proteins were detected by Western blot. Results:In K-ras silenced cell group, K-ras mRNA expression level decreased (80.5%±3.6%) and K-ras protein level decreased (58.9%±4.7%) when compared with the control group ( P<0.01) . Compared with the correspoding cell control group without exposure, the mRNA expression levels of c-myc, c-fos, N-ras and cyclin-D1 genes in HBE cell group exposed to different concentrations of PM 2.5, K-ras silenced cell group exposed to different concentrations of PM 2.5, HBE cell group exposed to 10 μmol/L Cr 6+ and K-ras silenced cell group exposed to 10 μmol/L Cr 6+ were increased, the mRNA expressions of p16 and p53 genes were decreased ( P<0.01) . Compared with HBE cell group exposed to 10 μg/ml PM 2.5, the mRNA expressions of c-myc, c-fos and p16 genes in K-ras silenced cells exposed to 10 μg/ml PM 2.5 were decreased, and the p53 mRNA level was increased ( P<0.01) . Compared with HBE cell group exposed to 50 μg/ml PM 2.5, the mRNA expression levels of c-fos, N-ras, cyclin-D1, p16 and p53 genes in K-ras silenced cell group exposed to 50 μg/ml PM 2.5 were decreased ( P<0.01) . Compared with the HBE cell group without exposure, c-myc protein increased and p53 protein decreased in HBE cells exposed to 50 μg/ml PM 2.5 ( P<0.05) . Compared with the K-ras silenced cell group without exposure, c-myc protein increased in K-ras silenced cells exposed to 50 μg/ml PM 2.5 ( P<0.05) . Conclusion:PM 2.5 can increase the expression levels of oncogenes in HBE cells, and K-ras gene silencing can inhibit the expression levels of oncogenes in HBE cells treated with PM 2.5.

Objective To analyze the clinical features,risk factors,imaging features and prognoses of cerebral infarction menifested as isolated acute vestibular syndrome (AVS) to improve the diagnoses and treatments of the disease.Methods Clinical data of 15 cerebral infarction patients menifested as isolated AVS,admitted to our hospital from October 2015 to April 2016,were summarized retrospectively.The clinical features,risk factors,imaging features and prognoses of these patients were analyzed.Results (1) Clinical characteristics:the average age of cerebral infarction patients menifested as isolated AVS was 62.1 ±13.5 years old,and the median attack time was 24 (4-168) h;the main clinical manifestations were vertigo,including nausea (n=1 1),vomiting (n=10),nystagmus (n=10),and unstable gait (n=14).(2) Risk factors:14 patients had multiple risk factors of stroke (＞4),and they were age,hypertension,hypedipidemia,diabetes,smoking,carotid stenosis,history of stroke,white matter degeneration,coronary heart disease,and atrial fibrillation.(3) Imaging features:14 patients were posterior circulation infarction,and the lesions were located in the cerebellar hemisphere (n=l 1),cauda cerebelli (n=4),pons (n=3),brachium pontis (n=1),brachium inferius cerebelli (n=1);inferior colliculus (n=1),and multiple lesions occurred in 6 patients;one anterior circulation infarction was located in the insula;most lesions were smaller lacunar infarcts,but the lower part of cerebellar hemisphere was mostly larger infarct.(4) Prognoses:the prognosis of patients is good after regular treatment,9 had complete symptom relief,and 6 got improvement.Conclusions When patients presented with isolated AVS and many risk factors exist in clinic,the possibility of cerebral infarction should be taken into account.Such patients should be subjected to relevant examinations in a timely manner and early diagnosis,so that they can get regular treatment as soon as possible and prognoses can be improved.

Objective:To analyze the pollution characteristics and source of fine particulate matter (PM 2.5) in Shenzhen and Taiyuan, two cities in the north and south of China. Methods:PM 2.5 samples were collected from the year of 2017 to 2018. The levels of 10 heavy metal elements (Pb, Al, As, etc.) , 10 water soluble ions (F -, Cl -, SO 42-, etc.) and 16 polycyclic aromatic hydrocarbons (PAHs) (Nap, Acy, Ace, etc.) in PM 2.5 were detected by inductively coupled plasma mass spectrometry (ICP-MS) , ion Chromatography and high Performance Liquid Chromatography respectively. USA commercial carbon analysis was applied to detect organic carbon (OC) and elemental carbon (EC) . Source of PM 2.5 was analyzed by Factor analysis method. Results:The concentrations of Pb, Mn, As, Ni, F -, OC and EC in PM 2.5 of Taiyuan city were significantly higher than those of Shenzhen City, and the concentrations of Na +, Cl -, and PO 43- were lower than those of Shenzhen City ( P<0.05) . Except naphthalene, the concentrations of PAHs in PM 2.5 of Taiyuan city were higher than those of Shenzhen City ( P<0.05) . The main sources of metal elements and water soluble ions in PM 2.5 in Shenzhen included: industry/vehicle exhaust factor (42.64%) , construction/soil factor (34.22%) and ocean factor (17.93%) . PAHs in PM 2.5 in Shenzhen mostly came from fuel oil/vehicle exhaust factor (38.58%) , coal combustion factor (30.78%) and biomass combustion factor (24.38%) . Differently, the main sources of metal elements and water soluble ions in PM 2.5 in Taiyuan included: construction factor (30.26%) , fuel oil and coal combustion factor (24.58%) , secondary particles/soil factor (22.03%) and industry factor (18.89%) . PAHs in PM 2.5 were from fuel oil/vehicle exhaust factor (54.71%) and coal combustion factor (43.54%) in Taiyuan. Conclusion:The sources of PM 2.5 pollution are different between Shenzhen and Taiyuan, the occupational health management must be continuously strengthened, measures should be strengthened contrapuntally on the basis of different pollution sources.

Objective:To construct the c-myc gene silenced hepatocytes, study the effect of c-myc gene silence on expression of oncogenes and apoptosis genes in hepatocytes treated with PM2.5.Methods:According to the c-myc gene mRNA sequence provided by GenBank, three interfering sequences were designed and synthesized, the recombinant lentiviral vector was transfected into L02 hepatocytes. The real-time quantitative PCR and western blotting were used to identify the effect of c-myc gene silencing. L02 cells and c-myc gene silenced cells were used as experimental subjects. The normal L02 cells and c-myc silenced cells were treated with 50 μg/ml PM 2.5 water soluble solution, 10 μM positive control Cr 6+ and a blank control, the treatment period was 24 h. The mRNA levels of oncogenes (c-myc, c-fos, k-ras, p53) and apoptotic genes (Caspase-3, Caspase-8, Caspase-9) were detected by real-time PCR. The protein levels of oncogenes and apoptotic genes were detected by western blotting. Results:The mRNA level and protein level of c-myc decreased by 81% and 70% in c-myc silenced cells when compared with the normal L02 hepatocytes, the above results indicate that c-myc gene silenced cells were successfully constructed. After c-myc silenced cells were treated with PM2.5 water soluble solution, The mRNA levels of c-myc, c-fos, and k-ras decreased by 84.1%, 45.4%, and 54.6% ( P<0.05) , p53 increased by 192.9% ( P<0.05) , and the expression of Caspase-3, Caspase-8, and Caspase-9 decreased by 24.4%, 36.1%, 60.9% ( P<0.05) . In the Cr 6+ positive control group, the expression of c-myc, c-fos, and k-ras decreased by 72.1%, 82.2%, and 54.0% ( P<0.05) , p53 increased by 250.0% ( P<0.05) , the expression of Caspase-3, Caspase-8, and Caspase-9 decreased by 34.6%, 36.0%, 68.9% ( P<0.05) , respectively, when compared with the normal L02 hepatocytes ( P<0.05) . Western blotting results showed that the protein levels of c-myc and c-fos increased, p53 decreased after PM 2.5 exposure; the protein levels of Caspase-3, Caspase-8, Caspase-9 increased after PM 2.5 exposure ( P<0.05) . When in comparison with the c-myc silenced group, the protein levels of c-myc and c-fos decreased, p53 protein increased in PM 2.5 exposed group ( P<0.05) . Conclusion:c-myc gene silenced cells were successfully constructed in this paper. PM 2.5 could promote the expression of oncogenes and apoptotic genes in L02 cells, and c-myc gene silencing can inhibit the expression of oncogenes and apoptotic genes after PM 2.5 treatment in L02 cells.

Objective:To study the effect of p38 mitogen-activated protein kinase (MAPK) gene silencing on expression of apoptotic genes and oncogenes in hepatocytes treated with PM 2.5. Methods:From June to September 2019, according to the p38MAPK gene mRNA sequence provided by GenBank, three interfering sequences were designed and synthesized, ligated into PLVX-shRNA2-puro after annealing, and the recombinant lentiviral vector was transfected into L02 hepatocytes. The p38MAPK silencing cells were identified by real-time fluorescent quantitative PCR and western blotting. The normal L02 cells and p38MAPK silencing cells were treated with 50 μg/mL PM 2.5 water soluble solution, 10 μmol/L positive control Cr 6+, and a blank control group was set up, the treatment time was 24 h. The mRNA levels of oncogenes (c-fos, c-myc, k-ras) , tumor suppressor gene (p53) and apoptotic genes (Caspase-3, Caspase-8, Caspase-9) were detected by real-time PCR. The protein levels of oncogenes and apoptotic genes were detected by Western blotting. Results:The expression levels of p38MAPK mRNA and protein in p38MAPK gene silencing cells were significantly lower than those in L02 hepatocytes ( P<0.05) , and the p38MAPK gene silencing cell line was successfully constructed. Compared with the blank control group, the expression levels of the oncogenes c-fos, c-myc, k-ras and the apoptosis genes Caspase-3, Caspase-8 and Caspase-9 increased, the expression level of tumor suppressor gene p53 decreased in the L02 hepatocyte group treated with PM 2.5 water soluble matter, and the differences were statistically significant ( P<0.05) . Compared with the L02 hepatocytes group treated with PM 2.5 water soluble matter, the expression levels of the oncogenes c-fos, c-myc, k-ras and apoptosis genes Caspase-3, Caspase-8 and Caspase-9 decreased, the expression level of tumor suppressor gene p53 increased in the p38MAPK gene silencing cells group treated with PM 2.5 water soluble matter, and the differences were statistically significant ( P<0.05) . Conclusion:PM 2.5 has effects on the expression of oncogenes, tumor suppressor genes and apoptotic genes in L02 hepatocytes, while p38MAPK gene silencing can inhibit the effects of PM 2.5 on L02 hepatocytes.

Objective:To analyze the pollution characteristics and source of fine particulate matter (PM 2.5) in Shenzhen and Taiyuan, two cities in the north and south of China. Methods:PM 2.5 samples were collected from the year of 2017 to 2018. The levels of 10 heavy metal elements (Pb, Al, As, etc.) , 10 water soluble ions (F -, Cl -, SO 42-, etc.) and 16 polycyclic aromatic hydrocarbons (PAHs) (Nap, Acy, Ace, etc.) in PM 2.5 were detected by inductively coupled plasma mass spectrometry (ICP-MS) , ion Chromatography and high Performance Liquid Chromatography respectively. USA commercial carbon analysis was applied to detect organic carbon (OC) and elemental carbon (EC) . Source of PM 2.5 was analyzed by Factor analysis method. Results:The concentrations of Pb, Mn, As, Ni, F -, OC and EC in PM 2.5 of Taiyuan city were significantly higher than those of Shenzhen City, and the concentrations of Na +, Cl -, and PO 43- were lower than those of Shenzhen City ( P<0.05) . Except naphthalene, the concentrations of PAHs in PM 2.5 of Taiyuan city were higher than those of Shenzhen City ( P<0.05) . The main sources of metal elements and water soluble ions in PM 2.5 in Shenzhen included: industry/vehicle exhaust factor (42.64%) , construction/soil factor (34.22%) and ocean factor (17.93%) . PAHs in PM 2.5 in Shenzhen mostly came from fuel oil/vehicle exhaust factor (38.58%) , coal combustion factor (30.78%) and biomass combustion factor (24.38%) . Differently, the main sources of metal elements and water soluble ions in PM 2.5 in Taiyuan included: construction factor (30.26%) , fuel oil and coal combustion factor (24.58%) , secondary particles/soil factor (22.03%) and industry factor (18.89%) . PAHs in PM 2.5 were from fuel oil/vehicle exhaust factor (54.71%) and coal combustion factor (43.54%) in Taiyuan. Conclusion:The sources of PM 2.5 pollution are different between Shenzhen and Taiyuan, the occupational health management must be continuously strengthened, measures should be strengthened contrapuntally on the basis of different pollution sources.