Effect evaluation of comprehensive reform of medical price in urban public hospital: A case study of Nanjing city / 中国卫生政策研究

Objectives:This study aims to analyze the change of income and medical service revenue of hospi-tals in Nanjing after the comprehensive reform of the medical prices of public hospitals,evaluate the effect of compen-sation and explore the differentiated compensation plan, and provide the basis for establishing the compensation mechanism of dynamic adjustment. Methods: A total of 10 municipal-affiliated hospitals were selected to collect fi-nancial income and expenditure data for the 48 months before the reform (2011.11—2015.10) and the 12 months after the reform(2015.11—2016.10) in Nanjing,and used interrupted time series model to estimate the growth rate of drug profit and service revenue,and finally made a comparison between the counterfactual and actual figures. Re-sults:It was found that,after the form,the drug profit decreased by 14.98%,and the service revenue increased by 24.79%. The revenue from medicines accounted for 42.7% and 36.9% before and after the reform respectively, and service for 28.9% and 30.3% respectively. The net financial aid accounted for 20.43% of the total drug-sales loss in average,and the net service revenue rate averaged 87.3% meeting the policy target,but within the 10 hospi-tals these rate ranged diversely from -21.9% to 712.5%,and 28.9% to 712.5%. The regression analysis indica-ted that the service compensation rate was significantly positively correlated with the proportion of service revenue in the total medical revenue before the reform. Conclusions:The Nanjing Pricing Reform basically achieved its desired goals of abolishing the drug-sales addition and the hospital compensation effect of 80% service +20% fiscal structure from service revenue and financial aid in average. However, the compensation differences among the hospitals are quite large with service-dependent hospitals compensated by over 400% and drug-dependent hospital less than 30%. However,for general hospitals,the compensation rated directly depended on the revenue structure before the reform and management performance and varied from 50% to 100%. The study at last gave its advices on improvement to further increase the service prices and establish a yearly-adjusted individualized compensation mechanism.

Tumor necrosis factor alpha affect hydrocortisone expression in mice adrenal cortex cells mainly through tumor necrosis factor alpha-receptor 1 / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Tumor necrosis factor alpha (TNF-α) is important in promoting relative adrenal insufficiency (RAI) due to systemic inflammatory response syndrome (SIRS). We identified the TNF-α receptor involved in the inhibition of adrenal corticotrophin (ACTH)-stimulated hydrocortisone release by studying the expression of TNF-α receptors in adrenal cortex Y1 cells and the effect of downregulating TNF receptors on ACTH-stimulated hydrocortisone release.</p><p><b>METHODS</b>We used real-time PCR and immunocytochemistry to evaluate the expression of TNF receptors on Y1 cells. TNF-receptor 1 (TNF-R1) DNA fragments corresponding to the short hairpin RNA (shRNA)-sequences were synthesized and cloned into pcDNA(TM) 6.2-GW/EmGFP expression vector. Knockdown efficiency of TNF-R1 expression was evaluated in miRNA transfected and mock-miRNA transfected Y1 cells by quantitative real-time PCR (Q-PCR). Hydro-cortisone expression levels were determined in TNF-R1-knockdown and control Y1 cells treated with TNF-α and ACTH.</p><p><b>RESULTS</b>Mouse adrenal cortex Y1 cells were positive for type I TNF-R1, but not type II TNF-receptor (TNF-R2). Blocking TNF-R1 expression resulted in loss of TNF-α-mediated inhibition of ACTH-stimulated hydrocortisone expression, suggesting a role for the TNF-R1 related signaling pathway in ACTH-stimulated hydrocortisone synthesis.</p><p><b>CONCLUSION</b>The inhibitory effect of TNF-α on ACTH-stimulated hydrocortisone synthesis was mediated via TNF-R1 in adrenal cortex.</p>

Effect of platelet-derived growth factor and lysosomes of lung injury in macaque with early-phase endotoxic shock / 中华急诊医学杂志

Objective To study the effect of platelet-derived growth factor(PDGF)and lysosomes on lung injury in macaque with early-phase endotoxie shock.Method Eleven macaques were randomly divided into two groups,namely,control group(Co group,n=5)iand endotoxic group(En group,n=6).The macaque of the Co group injected with 1 ml/kg normal saline and the macque of the En group received a dose of 2.8 mg/kg Lipopolysaccharides(LPS)i.v.The blood gas was detected at 120 minutes after LPS challenging. Uhrastructure,cytochemistry of acid phosphatase(ACPase)detection by electronic microscopy and immunohistochemical assay of PDGF were completed in hmgs of all the macaque .Results Administration of LPS did not change the parameters of gas exchange,namely,PaO_2,PaO_2/Fi and PaCO_2.In the early phase,of endotoxic shock,ACPase activity products increased and lysosome destroyed in the alveolar cells.The pathologic changes of alveolus,such as degeneration of vessel endothelium,injury of alveolar epithelium and damage of basement membrane,and transudation of blood component were observed by electron microscopy in the En group. However,no pathological changes were found in the control group.By immunohistochemical staining,PDGF on alveolar wall in the En animals was observed,whereas no PDGF protein in the Co macaques was noticed. Conclusions Administration of LPS induced the expression of PDGF in the alveolar wall and lysosome injury in the alveolar cells,as a result of alveolar damage in early-phase endotoxin shock.In the meantime,the parameters of gas exchanges did not change.The PDGF may play an important role in the pathogenesis of lung during the early-phase of endotoxin shock.