With the rapid increase in health cost and transformation of modern medicine, how to allocate the health care resources rationally and increase the efficiency and equity has become the common issues in all coun-tries. Health Economics, a new discipline, has provided possible answers to the issues and attracted attention from both government and academics. This paper introduces the goals, methods, contents and textbooks in US. universities and puts forwards suggestions for health economics education in China.

Epithelial-mesenchymal transition( EMT) refers to the transdifferentiation from epithelial cells to mesenchymal cells. The initial understanding of EMT is originated from the research on embryonic develop-ment,followed by the discovery of EMT phenomenon in physiological and pathological process in multicellular organism. In recent years,the occurrence and development of infiltration and metastasis of tumor cells along with fibrotic diseases that related to EMT are becoming the hot researches nowadays.

Objective To determine the dynamic changes of ileum epidermal growth factor(EGF),transforming growth factor-α(TGF-α)and epithelial growth factor receptor(EGFR)in neonatal rats with intestinal injury and to investigate their role in the neonatal necrotizing enterocolitis(NEC). Methods One-day-old Wistar rat pups were divided into two groups.The rats in the lipopolysaccharide(LPS)-injected group(n=40)received an intraperitoneal injection with 5 mg/kg LPS and those in the control group(n=8)did not.Control group and LPS-injected group at 1,3,6,12 and 24 h following LPS challenge were sacrificed for histological evaluation of NEC and for measurernents of EGF,EGFR,EGFR mRNA and TGF-α mRNA. Results Compared with the control group(0.12 0.17).the LPS-iniected pups showed a significant increase in injury scores at 1,3,6,12 and 24 h(1.28±0.62,1.75±0.74,1.98±0.75,2.85±0.41 and 2.35士0.63,respectively)(P<0.01).EGF protein levels at 1,3,6,12,24 h[(235.9±44.3)pg/mg prot,(231.8±30.0)pg/mg prot,(223.3±48.1)pg/mg prot,(211.7±47.0)pg/mg prot and(221.4±39.0)pg/mgprot,respectively]were significantly lower than that of the control group[(287.7±42.6)pg/mg prot](P<0.05).There was a negative correlation between the EGF levels and the grade of intestinal injury within 24 h(r=1.000,P<0.01).The expression of EGFR protein and mRNA was increased after LPS administration.There was no correlation between the EGFR protein and the grade of intestinal injury(r=0.800,P>0.05).The expression of TGF-α mRNA was significantly up-regulated at 1 and 3 h following LPS injection. Conclusions Reduced levels of EGF may play a pivotal role in the pathogenesis of NEC.

This paper reviews studies on the relationship between health insurance and health status both at home and abroad. First, we put forward three viewpoints on their relationship;Second, based on different data, we review the studies from three different perspectives; Third, we review the recent studies at home. The paper draws the conclusion as following:(1) most studies on observational data prove that there is relationship between health in-surance and health status. To establish the causal relationship between them, we must overcome the endogeneity of health insurance. ( 2 ) Different studies have different conclusions, which are caused by different methodology and subjects. (3)The conclusions cannot be generalized to whole populations. Future studies should focus on the effect of different health insurance on different populations.

Objective The early stage of neonatal sepsis is short of specific clinical manifestations that easy to be misdiagnosed.This study aimed to demonstrate the clinical value of combined markers[proca-icltonin(PCT)and C-reactive protein(CRP)]in the early diagnosis of neonatal hospital-acquired infections by dynamic monitoring of PCT and CRP.Methods The study included 111neonates in the 1st Neonatal Ward of Shengjing Hospital from June 2013to August 2014which were divided into three groups and retro-spectively reviewed,including 37cases of diagnosed sepsis group,42cases of clinical sepsis group,and 32ca-ses of control group(non-sepsis neonates).We measured the serum levels of PCT and CRP in two sepsis group before antibiotic administration,12h and 24h after infection,3d and 7d after infection controlled,and in the control group before antibiotic administration.Results Before antibiotic administration,serum levels of PCT and CRP were significantly higher in two sepsis groups than in the control group(P﹤0.01).In two sepsis groups,PCT reached peak at 12h after infection[(15.00±15.51)ng/ml and(17.93±13.44)ng/ml] and decreased to normal at 3d after infection controlled[(0.49±0.47)ng/ml and(0.42±0.34)ng/ml];CRP reached peak at 24h after infection[(37.53±30.29)mg/L and(32.41±29.33)mg/L]and decreased to normal at 7d after infection controlled[(5.72±2.98)mg/L and(5.06±3.07)mg/L].The optimal cut-off values were PCT﹥2ng/ml and CRP﹥10mg/L(Youden index 76.11%,59.45%),the sensitivity were 88.61%and 75.70% ;specificity were 87.5% and 83.75% ;positive predictive value were 94.59% and 95.65% ;negative predictive value were 75.68%and 46.15%.Receiver operating characteristic area under the curve were 0.964,0.887.Conclusion In early stage of sepsis,both PCT and CRP increase.The optimal cut-off values are CRP﹥10mg/L and PCT﹥2ng/ml.CRP reaches peak at 24h after infection,decrease to normal at 7d after infection controlled,while PCT reaches peak at 12h after infection,decrease to normal at 3d after infection controlled.Combined detection of PCT and CRP can improve the sensitivity and specificity of the early diagnosis of neonatal hospital-acquired infections.

0.05). However, the MDA level in the experimental group was higher than that of the control on day 3 [(55.92?5.53)nmol/mg prot vs (22.52?4.36)nmol/mg prot, P

Objective To explore the role of anterior horn index (AHI) in magnetic resonance imaging (MRI) outcome after intraventricular hemorrhage (IVH) and the correlation factors of IVH in preterm infants.Methods We selected 55 preterm infants with IVH(Ⅱ-Ⅳ degree) confirmed by MRI as case group,and 55 preterm infants with normal MRI as control group,all the cases were admitted in neonatal medical wards in our hospital from January 2009 to September 2011.Then 30 infants of case group were scaned for the second time,to see if they had posthemorrhagic ventricular dilatation (PHVD) and compare the AHI with the last time MRI,and analysis the related factors associated with IVH in preterm infants.Results MRI results:9 infants had PHVD,and the AHI rised (0.36 ± 0.05 v s 0.46 ± 0.06,P ＜ 0.01);21 infants didn't have PHVD,and the AHI decreased (0.31 ± 0.02 vs 0.30 ± 0.02,P ＜ 0.01).Logistic regression analysis:vaginal delivery,use of pulmonary surfactant,mechanical ventrilator care were associated with IVH (P ＜0.05).Conclusion AHI can be used for judging PHVD in preterm infants with IVH.Preterm infants with IVH,especially grade Ⅱ should be monitored AHI.Vaginal delivery and mechanical ventrilator may be risk factor of IVH in preterm infants,while use of pulmonary surfactant may a protective factor of IVH.

Objective To investigate the effect of hyperoxia on fluid transport by fetal distal lung epithelia(FDLE) and the expression of epithelial sodium channel(ENaC) in these cells.Methods FDLE were isolated and randomized into hyperoxia group and normoxia group,which were primarily cultured under hyperoxic or normoxic conditions,respectively.Fluid transport was measured using monolayers of FDLE cultured on Transwell permeable inserts.Western blot was applied to examine the α-ENaC expression.Results Fluid transport across monolayer of FDLE was increased in cells exposed to hyperoxia compaired with cells cultured in normoxic conditions (1.78 ± 0.19 vs 1.06 ± 0.11,P ＜ 0.001).Amiloride significantly decreased the fluid transport in both of the hyperoxia and normoxia groups,but in the presence of amiloride there were no difference between the two groups.The expression of α-ENaC was inhibited by hyperoxia to some extent(24h:0.44 ±0.04 vs 0.40 ±0.04,P=0.22; 48h:0.35 ±0.03 vs 0.47 ±0.06,P =0.03).Conclusion Hyperoxia enhanced total and amiloride-sensitive fluid transport by FDLE.However,the expression of α-ENaC decreased in these cells.

Objective To investigate the effect of hyperoxia on the transdifferentiation level of type Ⅱ alveolar epithelial cells (AEC Ⅱ) in vivo and in vitro,in order to illuminate the mechanism of epithelial injury in bronchopulmonary dysplasia (BPD).Methods Newborn Wistar rats were randomly devided into control group (room air inhalation) or model group (85％ oxygen inhalation) after birth.Lung tissue sampling and AEC Ⅱ isolation was conducted on 7 d,14 d,21 d.Type Ⅰ alveolar epithelial cells (AEC Ⅰ) marker aquaporin 5 (AQP5) and AEC Ⅱ marker surfactant protein C (SP-C) were examined by Western blot and florescent real-time PCR.AEC Ⅱ isolated from normal newborn rats was randomly devided into normoxia group (21％ oxygen) or hyperoxia group (85％ oxygen) after 24 h culture,and continued culturing for another 48 h in vitro.Then the morphological changes of cells were observed under inverted phase contrast microscope.The expression and location of markers for AEC Ⅰ and AEC Ⅱ was examined by immunofluorescence double staining.The protein expression of AQP5 and SP-C was evaluated by Western blot,and the mRNA expression of these markers was examined by florescent real-time PCR.Results In AEC Ⅱ isolated from the animal models,the AQP5 protein expression increased from 7 d while the SP-C expression decreased from 14 d in the model group comparing with the control group.In the model group,AQP5 mRNA expression increased and SP-C mRNA expression decreased since 7 d after hyperoxia exposure (P ＜ 0.05),with the difference between groups more obvious as exposure time extending.After culturing in vitro,AEC Ⅱ isolated from normal newborn rats expressed more AQP5 and less SP-C,with more cells double stained in the hyperoxia group compared with the normoxia group,examined by immunofluorescence double staining.The protein and mRNA examination results both showed that AQP5 expression increased and SP-C expression decreased in the hyperoxia group compared with the normoxia group (P ＜0.01).Conclusion After hyperoxia exposure,no matter in vivo or in vitro,the expression of AEC Ⅱ marker SP-C decreases while the expression of AEC Ⅰ marker AQP5 increases.These results indicate that the excessive transdifferentiation of AEC Ⅱ takes part in the recovery process after hyperoxia induced lung injury.

Objective To investigate p16 promoter methylation in premature rats with chronic lung disease induced by hyperoxia. Methods Eighty premature Wistar rats were randomly divided into two groups: hyperoxia group (fraction of inspiratory oxygen) 0. 90 and control group (fraction of inspiratory oxygen 0. 21), 40 rats for each group. Semi-nested methylation specific polymerase chain reaction and methylation specific polymerase chain reaction were applied respectively to detect p16 promoter methylation in lung tissues. Additionally, p16 mRNA and protein expressions in lung tissue were detected by reverse transcription- polymerase chain reaction, Western blot and immunohistochemistry method. Results The methylation was not found in control group by seminested methylation specific polymerase chain reaction and methylation specific polymerase chain reaction, while was found in different aged rats of the hyperoxia group. The methylation detection rate was higher by using the semi-nested methylation-specific polymerase chain reaction (52.5%, 21/40) than that by methylation specific polymerase chain reaction (42.5%, 17/40) in the hyperoxia group,but there was no statistically significant difference between the two methods. The p16 mRNA in the hyperoxia group were significantly lower than in the control group at day 7, 14 and 21(1.73 ± 0.40 vs 2.11±0. 37,1.29±0. 19 vs 1.60±0. 27,0. 95±0.25 vs 1.72±0. 34, t=2.19, 2.95 and 10. 43,P＜0. 05). The p16 protein expressions by western blot in the hyperoxia group were significantly lower than in the control group at day 7, 14 and 21 also (88. 1±8. 7 vs 95.0±4.1,65.7±4.5 vs 83. 5±13.6 and 50.4±4.9 vs 86.7±11.9, t=2.27,3.95 and 13.40,P＜0.05). The expression of p16 mRNA (1.06±0.61) and protein (62.32±25.65) in lung tissues of rats with methylation was lower than that without methylation (1.63±0.62 and 94.93±22.21, respectively) (t=2.95, OR=0. 86;t=4.28, OR=0. 85,P＜0.01, respectively). Conclusions Exposure to hyperoxia might induce p16 promoter methylation in lung tissues in premature rats. Methylation risk increases as exposure time extends. p16 promoter methylation induced by hyperoxia might participate in the mechanism of lowering p16 mRNA and protein expression, but might not result in p16 gene silence.