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.

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.

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

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 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.

Objective To investigate the correlation between brain injury and premature infants with bronchopulmonary dysplasia (BPD)and to analyze the risk factors of brain injury in premature infants with BPD based on MRI changes.Methods A total of 1 13 premature infants diagnosed with BPD were studied as case group from January 2010 to December 2014 at the neonatal ward of Shengjing Hospital of China Medical University.One hundred and sixty-two premature infants without BPD were selected as control group.There were no significant differences in gestational age and birth weight between the two groups.All cases were per-formed MRI examination in hospital.The occurrence of brain injuries(white matter injury and intracranial hemorrhage)were compared based on MRI changes between the two groups,and the risk factors of brain in-jury in case group were analyzed.Results The case group and control group were performed MRI on (33.73 ±16.00)d,(24.40 ±12.29)d after birth respectively.The ratio of brain injury,intracranial hemor-rhage,cerebral white matter damage and severe brain injury of case group was higher than those of the control group(48.7% vs.32.7%,3 1.9% vs.21.6%,31.9% vs.21.6%,16.8% vs.8.6%,respectively).The differences were significant in the ratio of brain injury and severe brain injury (P =0.008,P =0.040,respec-tively).Logistic regression analysis showed that postnatal infection was a risk factor for brain injury of the case group(OR =2.21 ,95%CI 1.04 ~4.72,P ﹤0.05).Conclusion More brain injury(including the white matter injury and intracranial hemorrhage)and severe brain injury(including grade III ~IV intraventricular hemorrhage and periventricular leukomalacia)are detected in premature infants with BPD.Postnatal infection is a risk factor of brain injury for premature infants with BPD.

miRNAs are a group of 22 ~25 nucleotides endogenous non-coding RNAs,which regulate gene expression at the post-transcription level by cause the degradation or translational suppression of target mR-NAs.In recent years,studies have demonstrated that miRNAs widely participate in cell differentiation,prolifera-tion,organ development and lipid metabolism,and are closely related to the formation of many kinds of diseases. The biological function of miRNAs and their effects on regulating prenatal and postnatal lung development are reviewed in this paper.

Objective To investigate the variation in expression and the significance of markers indi-cating typeⅠalveolar epithelial cells ( AECⅠ) and type Ⅱ alveolar epithelial cells ( AECⅡ) in hyperoxia induced bronchopulmonary dysplasia( BPD) model. Methods A total of 80 term normal Wistar rats were randomly devided into model group (85% oxygen) or control group (room air) within 12 h after birth,with 40 rats in each group. On day 7,day 14,day 21 after exposure,the pathological characteristics of lung tissues were observed using HE staining, the expression and location of AECⅠ marker aquaporin 5 ( AQP5 ) and AECⅡmarker surfactant protein-C ( SP-C) were examined using immunofluorescence double staining. West-ern blot analysis was employed to examine the expressions levels of AQP5 and SP-C proteins,while real-time PCR was used to evaluate the mRNA expression of AQP5 and SP-C. Results Alveolar developmental disor-der was observed in lung tissues of the model group,including fewer,larger,simplified alveoli,thicker alveo-lar walls,and fewer alveolar secondary septa. Immunofluorescence double staining showed increased and dis-organized AQP5 and SP-C expression, with significantly higher ratio of double-stained cells/SP-C positive cells in the model group ( P<0. 001 ) . Comparing to the control group, the expression of AQP5 and SP-C protein increased from 7 d after hyperoxia exposure,which continued to 21 d. The mRNA expression levels of these two markers both significantly increased in the model group compared with the control group, with AQP5 starting from 7 d while SP-C starting from 14 d after hyperoxia exposure (P<0. 05),and the differ-ence between two groups became more significant with the exposure time extending. Conclusion The expression of AECⅠ marker AQP5 and AECⅡ marker SP-C both increase in the lung tissues of hyperoxia induced BPD newborn rats,with more AECⅡ transdifferentiated into AECⅠ. These changes of the markers indicate that there is excessive transdifferentiation of AECⅡ in the recovery process after BPD 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.