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Objective To explore the feasibility of various compensation approaches and their combination after canceling the drug addition at municipal public hospitals in Anshan city.Methods 2008~201 1 medical services,balance of payments of Anshan municipal public hospitals during 2008~201 1 were analyzed,to calculate the balance of profit and loss of the hospitals with the drug addition canceled,as well as the effects of various compensation models and their combinations on hospitals’balance,government financial burden,costs of health insurance and patients’out-of-packet costs.Results Without drug addition,hospitals are found with surplus drop,and doubled number of years in deficit.Losses incurred by the canceling can be covered partly by pricing adjustment of medical services or collection of pharmaceutical service surcharge,with complete compensation by collection of medical service surcharge;government financial subsidies for large equipment depreciation or medical services offer part of the compensation,which is affordable by government finance.Such deficits cannot be covered completely by any single approach,yet they can be greatly eased by a combination of the approaches mentioned above.With impacts on all stakeholders in consideration,the optimal solution is the combination of the scheme with adjusted services price plus collection of pharmaceutical service surcharge and medical services compensation.Conclusion With the drug addition policy canceled,the establishment and perfection of the compensation mechanism calls for a synergy of pricing,health insurance and government finance.
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This review firstly introduces sixty h type indices which are categorized in order to overcome the drawbacks of the Hirsch index,especially the advantages and limits of the h type indices when comparing with h index.Moreover,the review gives a list to show the main characteristics of h type indices.Lastly,some illustrative researches are shown to present the applicability of some h type indices.
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Objective To explore and establish an evaluation index system of clinical departments' medical work performance mainly based on workload and the quality of work. Methods Literature method and a variety of statistical methods were applied to establish index system, the principal component analysis and TOPSIS method were used to give an statistical analysis. Results There was a positive correlation between the comprehensive evaluation value of medical work performance of non-surgical and surgical departments and the balance of financial revenue and expenditure of the departments. The pearson correlations of these two kinds of departments were 0.570 and 0.287, and the non-parametric correlations were 0. 427 and 0.566. Conlusion The index system and evaluation results of this study can provide reference for the allocation of allowances.
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<p><b>BACKGROUND</b>Cluster of differentiation 44 (CD44) is a family of transmembrane glycoproteins. As cell surface hyaluronate receptor, it has been found to be widely expressed in a variety of cells. The aim of this study is to assess the relationship among CD44 expression, DNA content, proliferation index (PI) and apoptosis in female adenocarcinoma of the lung.</p><p><b>METHODS</b>The expression of CD44, DNA index (DI), PI and apoptotic rate were studied in 61 cases of female adenocarcinoma of the lung, paracancerous tissues and 45 cases of benign lesions by flow cytometry.</p><p><b>RESULTS</b>The percent of DNA aneuploidy was 75.41% in adenocarcinoma. The expression of CD44, DI and PI in adenocarcinoma were significantly higher than those in paracancerous and benign controls (P < 0.01), however the apoptotic rate was obviously lower in adenocarcinoma than that in paracancerous and benign controls (P < 0.01). There was a positive correlation between CD44 and DI (P < 0.01), and a negative correlation between apoptosis and DI in adenocarcinoma (P < 0.01).</p><p><b>CONCLUSIONS</b>The expression of CD44, DNA content, proliferation and apoptosis may play important regulating roles in oncogenesis, development and metastasis of female adenocarcinoma of the lung.</p>
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<p><b>BACKGROUND</b>Xeroderma pigmentosum group D (XPD) is one of the important DNA repair genes. XPD polymorphism at Lys751Gln site has been shown to alter XPD protein function, modulate DNA repair capacity and therefore affect cancer risk. The aim of this study is to explore the relationship between XPD polymorphism and susceptibility to lung cancer in nonsmoking female via a population-based case-control study.</p><p><b>METHODS</b>There were 105 female patients who were diagnosed with lung cancer between January 2004 and December 2005 from Liaoning Tumor Hospital and 202 Hospital, and the control group included 105 healthy volunteers who were obtained from community centers at the same time. Information concerning demographic and risk factors was obtained for each case and control by a trained interviewer. XPD genotypes of cases and controls were determined by PCR-RFLP method. Two-sided Chi-Square test was used to compare the distribution of the genotypes and risk factors between cases and controls. Unconditional logistic regression analysis was performed to calculate the odds ratios (OR) with 95% confidence intervals (CI) for estimating the association between certain genotypes and lung cancer and exploring the interaction of environmental risk factors and genetic polymorphism.</p><p><b>RESULTS</b>All of the subjects in this study were nonsmoking females in Shenyang. There was no significant demographic difference (age, economic level and education) between cases and controls. There was a significant difference in the frequencies of XPD polymorphism between cancer cases and controls. The frequencies of XPD 751Gln allele were 6.2% in controls and 13.8% in cases (P < 0.05). The risk of lung cancer was higher in those with the Lys/Gln or Gln/Gln genotype than in those with the Lys/Lys genotype and adjusted OR was 2.80 (95% CI: 1.21-6.48). The result showed that cooking fumes exposure was a risk factor for lung cancer (OR was 2.44). Furthermore, an interaction between environmental risk factors and the variant XPD 751Gln allele on the risk of lung cancer was observed. Individuals with both risk gen-otype and exposure to cooking fumes had a higher elevated risk of cancer than those with only one of them (adjusted OR= 6.85 ; 95% CI: 1.69-27.67; P=0.007).</p><p><b>CONCLUSIONS</b>The above findings indicate that the Lys751Gln polymorphism in XPD gene is associated with the risk of lung cancer in nonsmoking females. Individuals with both XPD 751Gln allele genotype and exposure to cooking fumes have a higher elevated risk of cancer than those with only one of them in nonsmoking female population.</p>
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<p><b>BACKGROUND</b>XRCC1 polymorphism at Arg399Gln site has been shown to modulate DNA repair capacity. The aim of this study is to assess the relationship between XRCC1 polymorphism and susceptibility to lung adenocarcinoma in nonsmoking female via a hospital-based case-control study.</p><p><b>METHODS</b>Cases were 126 female patients with lung adenocarcinoma from January 2002 to October 2004 in China Medical University Hospital and Liaoning Tumor Hospital. Controls were selected from patients with other pulmonary diseases in the hospitals at the same time. These controls were matched to cases on age (±5 years). Information concerning demographic and risk factors was obtained for each case and control by a trained interviewer. XRCC1 genotypes were determined by PCR-RFLP. The adjusted odds ratio (OR) and 95% confidence interval (CI) were calculated using logistic regression.</p><p><b>RESULTS</b>Cases showed a higher prevalence of oil smoke compared with controls (P < 0.05). The frequencies of Arg/Arg, Arg/Gln and Gln/Gln in lung adenocarcinoma group (32.54%, 42.86%, 24.60%) were significantly different from those in controls (54.76%, 40.48%, 4.76%) (P < 0.05). The individual carrying Gln/Gln genotype was at a significantly increased risk of lung adenocarcinoma compared with those with Arg/Arg genotype (OR=8.695, 95%CI 3.343-22.614, adjusted for age and oil smoke exposure). Furthermore, the OR of lung adenocarcinoma for the variant XRCC1 399Gln allele combined with exposure to oil smoke was 5.21 (95%CI 1.85-14.70, P < 0.001).</p><p><b>CONCLUSIONS</b>The results indicate that the Arg399Gln polymorphism in XRCC1 is associated with the risk of lung adenocarcinoma in nonsmoking women.</p>
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<p><b>BACKGROUND</b>Lung cancer is a serious health problem in public. Its morbidity and mortality have been increasing rapidly. The mortality of lung cancer in women also increases year by year, in which most of the cases are non-smoking women, and the risk factors still are unclear. The aim of this study is to explore the effects of air pollution in room, passive smoking and other factors on risk of lung cancer.</p><p><b>METHODS</b>A total of 618 newly diagnosed female patients with primary lung cancer were enrolled. The controls were selected randomly in the general population in urban districts. Two trained interviewers performed this interview face-to-face using the same questionnaire. The content of questionnaire included the characteristics of demography, history of passive smoking, exposed history of cooking fume, fuel exposure, exposed history of coal fume, history of using 'Kang', pulmonary disease history, cancer history of relatives and occupational history.</p><p><b>RESULTS</b>Passive smoking in childhood was related with lung cancer of non-smoking women (OR= 1.81 , 95%CI=1.46-2.24). The exposure to the cooking fume was of great significance (OR=3.18, 95%CI= 2.55 -3.97). The relationship between coal fume and lung cancer was significant (OR=2.56, 95%CI= 1.83 -4.55). The pulmonary disease history including tuberculosis, chronic bronchitis, asthma, pneumonia, emphysema was strongly associated with lung cancer (OR=1.80, 95%CI=1.43-2.27). The family history of cancer significantly increased the risk of lung cancer (OR=2.09, 95%CI=1.46-3.00), especially the lung cancer history in the first relatives (OR=2.46, 95%CI=1.55-3.90). After adjusting other factors, logistic analysis showed that cooking fume (OR=4.11, 95%CI=2.14-7.89), the pulmonary disease history (OR= 2.05 , 95%CI=1.08-3.93), and the family history of lung cancer (OR=2.89, 95%CI=1.30-6.41) were significant factors.</p><p><b>CONCLUSIONS</b>The results show that passive smoking in childhood, cooking oil exposure, coal fume exposure, pulmonary disease history including tuberculosis and family history of lung cancer are risk factors of lung cancer in non-smoking women.</p>
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<p><b>BACKGROUND</b>To explore the relationship between the expression of COX-2 and pathophysiological features in female pulmonary adenocarcinoma patients.</p><p><b>METHODS</b>Expression of COX-2 protein was detected in 50 cases of female pulmonary adenocarcinoma tissues and 50 cases of paracancerous tissues by streptavidin-biotin immunoperoxidase method.</p><p><b>RESULTS</b>The positive rates of COX-2 expression were 78% and 26% in tumor tissues and paracancerous tissues respectively, and there was a highly significant difference between the two groups (Chi-square=27.08, P < 0.01). No significant difference was found among COX-2 expression level, age (P=0.50), smoking history (P=1.0), differentiation grade of tumor cells (P=0.712), TNM stage (P=0.591), size of primary tumor (P=0.63) and lymph nodes metastasis (P=0.88).</p><p><b>CONCLUSIONS</b>Overexpression of COX-2 may play an important role in oncogenesis of female lung adenocarcinoma.</p>