Gastric cancer is a kind of disease with high incidence and mortality rate,most gastric cancer cases are diagnosed in an advanced,and chemotherapy is the main treatment.Drug resistance is one of the most important causes of therapy failure in gastric cancer patients.It has revealed that the mechanism of tumor resistance mainly involves alterations in cell cycle and proliferation,enhanced DNA repair capacity,defective apoptosis,damaged host immune,altered metabolism of drugs and so on.In recent years,an important molecule-microRNA(miRNA)that regulates the biological behavior of cell has attracted more and more attention.Studies have confirmed that numerous miRNAs can regulate the drug resistance of gastric cancer cells via BCL-2 signaling pathway,PTEN/PI3K/AKT pathway,ABCB1(MDR1/P-gp),autophagy,cell cycle and so on.

Objective To observe the diagnostic value of telomerase,VEGF,CD44_ V6 ,MMP_2,MMP_9and their combined examination in distinguishing malignant pleural effusion from benign one.Methods Sixty patients with pleural effusions were observed,thirty of them sufferring from malignant pleural effusion and thirty of them sufferring from benign one.The expression of telomerase,CD44_ V6 ,VEGF,MMP_2,MMP_9were tested in the pleural effusion by RT-PCR and ELISA technique.The sensitivity and the specificity of each examination method were calculated,in order to find out appropriate combination.Results As single-item detection,the diagnosetic value of VEGF was the best,the cutoff of VEGF was 181.1pg/ml,the sensitivity of VEGF examination was 90.0%,and the specificity was 86.7%.The sensitivity and the specificity of combined examination VEGF+CD44_ V6 and VEGF+MMP_2 were the best,the sensitivity of VEGF+CD44_ V6 was 83.3%,and the specificity was 90.0%.The sensitivity of VEGF+MMP_2 was 80.0% and the specificity was 93.3%.Conclusion The level of telomerase,VEGF,CD44_ V6 ,MMP_2,MMP_9in malignant pleural effusion is clearly higher than that in benign pleural one,the difference having significant statistic meaning.VEGF has higher sensitivity and specificity .Of combined examination,VEGF+CD44_ V6 and VEGF+MMP_2 have higher sensitivity and specificity.

Objective:To explore the changes of neuron-specific enolase (NSE) and S-100β protein (S-100β) during perioperative period in infants undergoing living liver transplantation and examine the effect of brain injury.Methods:From January 2015 to January 2016 in Department of Anesthesiology First Central Clinical College Tianjin Medical University, study group was composed of forty infants of congenital biliary atresia with an age range of (4-12) months, a body weight of (4-10) kg and American Society of Anesthesiologists (ASA) class Ⅲ/Ⅳ. Another 40 infants undergoing general surgery were selected as control group. In study group, blood samples were harvested from central vein pre-operation (T0), before skin incision (T1), 30 min after anhepatic phase (T2), 1 h of neohepatic phase (T3) and 24h after hepato-reperfusion (T4). In control group, blood samples were collected at pre-operation (T0) and 24 h post-operation (T4). Serum levels of S-100β, NSE, heart rate (HR), mean arterial blood pressure (MAP), central venous pressure (CVP) and bispectral index (BIS) were monitored at T1-4 and end of surgery. All children were assessed by Bayley Scale of Infant Development (BSID) at Day 1 pre-operation and 2/4 weeks post-operation for observing mental and motor development status. The results were described with mental development index (MDI) and psychomotor development index (PDI). Pediatric anesthesia emergence delirium (PAED) was employed for evaluating the severity of delirium during the recovery stage at 30 min and 2/4h post-extubation.Results:In study group, serum levels of S-100β and NSE changed significantly during non-hepatic and neohepatic reperfusion phases. After inferior vena cava occlusion, serum concentrations of S-100β and NSE spiked ( P<0.05) and gradually recovered during neohepatic reperfusion period ( P<0.05). No significant inter-group difference existed in serum S-100β or NSE at T4 ( P>0.05). In study group, as compared with Day 1 pre-operation, MDI/PDI decreased at Week 2 post-operation ( P<0.05) and increased from Month 1 post-operation ( P<0.05). Both MDI and PDI were lower than control group before and at Week 2 post-operation ( P<0.05). MDI/PDI of study group basically reached the preoperative level at Month 1 post-operation ( P<0.05). In control group, no significant difference existed in MDI/PDI at Day 1 pre-operation and Week 2/4 post-operation ( P>0.05). In study group, the delirium rate was up to 30% post-extubation and decreased at 2/4h post-extubation. In control group, the incidence of delirium was low at 30 min and 2/4h post-extubation ( P<0.05). Conclusions:Perioperative evaluations of serum levels of NSE and S-100β are significant for predicting the postoperative onsets of delirium and cognitive impairment in children with living donor liver transplantation.

Objective By detecting the variation of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) DNA methylation in preeclampsia-like mouse models generated by different ways, to explore the roles of multifactor and multiple pathways in preeclampsia pathogenesis on molecular basis. Methods Established preeclampsia-like mouse models in different ways and divided into groups as follows: (1) Nw-nitro-L-arginine-methyl ester (L-NAME) group: wild-type pregnant mouse received subcutaneous injection of L-NAME;(2) lipopolysaccharide (LPS) group:wild-type pregnant mouse received intraperitoneal injection of LPS; (3) apolipoprotein C-Ⅲ (ApoC3) group: ApoC3 transgenic pregnant mouse with dysregulated lipid metabolism received subcutaneous injection of L-NAME;(4)β2 glycoprotein I (β-2GPI) group:wild-type pregnant mouse received subcutaneous injection ofβ-2GPI. According to the first injection time (on day 3, 11, 16 respectively), the L-NAME, LPS and ApoC3 groups were further subdivided into:pre-implantation (PI) experimental stage, early gestation (EG) experimental stage, and late gestation (LG) experimental stage.β-2GPI group was only injected before implantation. LCHAD gene methylation levels in placental were detected in different experimental stage. Normal saline control groups were set within wild-type and ApoC3 transgenic pregnant mice simultaneously. Results (1) CG sites in LCHAD DNA:45 CG sites were detected in the range of 728 bp before LCHAD gene transcription start site, the 5, 12, 13, 14, 15, 16, 19, 24, 25, 27, 28, 29, 30, 31, 32, 34, 35, 43 CG sites were complex sites which contained two or more CG sequences, others were single site which contained one CG sequence. The 3, 5, 6, 11, 13, 14, 18, 28 sites in L-NAME, LPS, ApoC3 and β-2GPI groups showed different high levels of methylation; the 16, 25, 31, 42, 44 sites showed different low levels of methylation; other 32 sites were unmethylated. (2) Comparison of LCHAD gene methylation between different groups:the methylation levels of LCAHD gene at 3, 11, 13, 14, 18 sites in L-NAME, LPS, ApoC3 andβ-2GPI groups were significantly higher than those in the normal saline control group (P<0.05); and the methylation levels of 42, 44 sites in these groups were significantly lower than those in the normal saline control group (P<0.05). (3) Methylation of LCHAD gene at the same site between different experimental stages: ① The 3, 11, 18 sites of EG experimental stage was significantly lower than PI and LG experimental stage in L-NAME group (P<0.05);the 3, 11, 18 sites of PI experimental stage was significantly lower than EG and LG experimental stage in LPS group (P<0.05);these sites of PI experimental stage was significantly higher than EG and LG experimental stages in ApoC3 group (P<0.05).②The methylation of site 5 in L-NAME and LPS groups were significantly higher than that of the normal saline control group (P<0.05), and the LG experimental stages were significantly higher than other stages, but in ApoC3 group , only PI and EG stages were significantly higher than the normal saline control group (P<0.05).③At site 6 in L-NAME group which showed high methylation level was significantly higher than the same site in other groups which showed low methylation level (P<0.05).④At 13, 14 sites, earlier preeclampsia onset caused a lower methylation level in L-NAME group, but PI experimental stage was significantly higher than EG and LG experimental stages in LPS group (P<0.05), EG experimental stage was significantly higher than PI and LG experimental stages in ApoC3 group (P<0.05). ⑤ At site 28, earlier preeclampsia onset caused a higher methylation level in L-NAME group, but PI experimental stage was significantly lower than EG and LG experimental stages in LPS group (P<0.05), EG experimental stage was significantly higher than PI and LG experimental stages in ApoC3 group (P<0.05).⑥The 16, 25, 31 sites in ApoC3 group were significantly higher than other groups (P<0.05). ⑦ At site 42 in β-2GPI group was unmethylated, but it in other groups showed low methylation level, the methylation level of site 42 inβ-2GPI group was significantly lower than that in other groups (P<0.05). Conclusions The methylation of 6 and 42 CG sites may be related to LCHAD gene expression in placenta of L-NAME and β-2GPI induced preeclampsia-like models respectively;LCHAD gene expression and DNA methylation may not have obviouscorrelation in LPS and ApoC3 induced preeclampsia-like models. Differences exist in LCHAD DNA methylation in preeclampsia-like models generated by different ways, revealed a molecular basis to expand our understanding of the multi-factorial pathogenesis of preeclampsia.

Objective To evaluate the relationship between 18F-FDG uptake and P-gp expression in Bcap37 or Bcap37/MDR1 tumor-bearing BALB/c nude mice.Methods Bcap37 or Bcap37/MDR1 cells were injected into BALB/c nude mice (1× 107cells/ml,0.2 ml/mouse) to construct mice models.Bcap37 (n=5) or Bcap37/MDR1 (n=5) tumor-bearing mice fasted for 6 h before imaging.After anesthesia,the mice were injected with 7.4 MBq of 18F-FDG via tail vein.The dynamic microPET scans were carried out for 90 min.On the microPET images,the ROI was drawn and the TAC was obtained.The next day,those 10 mice underwent dynamic microPET scans after injected with elacridar (GF120918) and 18F-FDG.Another 10 mice,5 with Bcap37 tumors and 5 with Bcap37/MDR1 tumors,were used.After 7.4 MBq 18F-FDG with or without 2.0 mg/kg GF120918 was administered via tail vein,microPET images were acquired at 60 min.ROI was drawn over the tumors and SUV was obtained.Two-sample t test was used to analyze the data.Results GF120918 did not significantly alter the 18F-FDG accumulation curve in Bcap37 tumors,but significantly enhanced the 18F-FDG accumulation in Bcap37/MDR1 tumors.GF120918 did not influence 18F-FDG uptake (SUV) in Bcap37 tumors (1.052±0.028,1.028±0.045,t =1.792,P＞0.05),but significantly increased the SUV in Bcap37/MDR1 tumors (1.015±0.043,0.712±0.031,t=3.365,P＜0.05);The SUV of 18 F-FDG in Bcap37 tumors was significantly higher than that in Bcap37/MDR1 tumors without injection of GF120918 (t =3.952,P＜0.05).The SUV was not significantly different when GF120118 was injected (t=1.835,P＞0.05).Conclusions 18F-FDG is a substrate of P-gp.18F-FDG imaging combined with GF120918 injection may be an effective noninvasive method for the detection of tumor's MDR.

Objective To evaluate the effect of P-gp inhibitors of verapamil (VER) and GF120918 on 18F-FDG uptake in Bcap37 and Bcap37/multidrug resistancce (MDR)1 cell lines in vitro,and to explore the relationship between 18F-FDG uptake and P-gp expression at cellular level.Methods Bcap37 and Bcap37/MDR1 cells were seeded into 6-well plates at a density of 1 × 106 per well.Three days later,37 kBq/ml 18F-FDG,or 37 kBq/ml 18F-FDG + 100 μmoL/L VER,or 37 kBq/ml 18F-FDG + 50 μmol/L GF120918 were added into each well.Mter incubated for 10,30,60 and 120 min at 37 ℃ and in 5％ CO2,the medium was removed and the cells were washed three times with 1 ml ice-cold PBS immediately.The radioactivity of 18 F-FDG was measured using a gamma counter.The uptake of 18F-FDG was expressed as the ratio of 18F-FDG radioactivity in Bcap37 or Bcap37/MDR1 cells and the overall radioactivity added to the cells in each well.The t test was used for statistical analysis.Results 18F-FDG uptake was higher in Bcap37/MDR1 cells than that in Bcap37 cells after incubated for 10 min.The uptake rate was (1.88 ±0.19) ％ in Bcap37/MDR1 cells and (1.37 ± 0.18) ％ in Bcap37 cells (t =7.832,P ＜ 0.05).On the contrary,18 F-FDG uptake was significantly higher in Bcap37 cells than that in Bcap37/MDR1 cells after incubated for 60 and 120 min.The uptake rates were (2.29 ±0.23)％ and (2.34 ±0.15)％ in Bcap37 cells,(1.47 ±0.14)％ and (1.53 ±0.22)％ in Bcap37/MDR1 cells (t =8.437,8.283,both P ＜ 0.05).18 F-FDG uptake was significantly higher with VER or GF120918 in Bcap37/MDR1 cells than that without VER or GF120918 after the incubation of 60 and 120 min (t =9.032,9.243 and 8.765,8.803,all P ＜ 0.05).The uptake rates with VER or GF120918 were (2.45 ±0.21)％ and (2.46 ±0.25)％,(2.50 ±0.24)％ and (2.48 ±0.27)％.There was no significant difference of 18F-FDG uptake in Bcap37 cells with or without VER or GF120918.Conclusions 18F-FDG is a substrate of P-gp at cellular level.P-gp may act as an efflux pump to reduce 18F-FDG uptake in Bcap37/MDR1 cells.The uptake of 18F-FDG can be used to evaluate the function of P-gp in tumor cells.

Objective To explore the effects of impaired glucose metabolism and impaired blood lipoprotein metabolism on heart rate variability(HRV) in aged male hypertension patients and to have an insight into the correlation between the years of impaired glucose metabolism and the patients’ HRV. Methods 120 male subjects were divided into three groups: simple hypertension patients (group A, 40 people), hypertension patients with diabetes mellitus (group B, 40 people), and hypertension patients with diabetes mellitus and impaired blood lipoprotein metabolism (group C, 40 people). All subjects had 24h recordings of ECG. The data of HRV time domain were collected and analyzed to gain an insight into the effects of the impaired glucose metabolism and impaired blood lipoprotein metabolism on patients’ HRV. In group C, patients were divided into normal TC subgroup and high TC subgroup according to the index of TC (TC

Objective To analyze the level of cardiac troponin I (cTnI) in children with left-to-right shunt congenital heart disease (CHD). Methods In this study, 146 children with secundum atrial septal (ASD) defect, 132 children with ventricular septal defect (VSD) and 300 healthy children were recruited. The levels of cTnI and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured and their correlation with clinical data was analyzed. Results The serum cTnI and NT-proBNP levels in both ASD and VSD patients were signiifcantly higher than those in normal children (H=3.89 and 5.27, P<0.01). The serum cTnI and NT-proBNP levels in VSD patients were signiifcantly higher than those in ASD patients (P<0.05). The ratio of pulmonary to systemic arterial pressure (Pp/Ps), pulmonary vascular resistance index (PVRI) and standardized left ventricular end diastolic volume in VSD patients were signiifcantly higher than those in ASD patients (P<0.05). Multiple regression analysis showed that Pp/Ps was signiifcantly correlated with cTnI in VSD patients. (β=0.81, SE=0.03, P=0.000). Conclusions Signiifcant volume and pressure overload due to a left-to-right shunt induce myocardial injury and could lead to irreversible myocardial remodeling in children with CHD. The serum cTnI level is a sensitive biomarker for myocardial damage in VSD patients.

Objective To evaluate the effect of propofol on brain injury during hepatic ischemiareperfusion (I/R) in preadolescent mice.Methods Forty-eight healthy male C57BL/6 mice.aged 2 weeks,weighing 6-9 g,were allocated to one of 3 groups (n=16 each) using a random nunber table:sham operation group (group S),hepatic I/R group (group I/R) and propofol group (group P).Hepatic I/R was produced by occlusion of the blood supply to the median and left lobes of the liver for 60 min followed by reperfusion in anesthetized mice.In group P,1％ propofol 30 mg/kg was intraperitoneally injected at 30 min before skin incision,while the equal volume of normal saline was given instead in S and I/R groups.Blood samples were collected and brains were removed at 24 h of reperfusion,and hippocampi were then isolated.The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in hippocampi and levels of TNF-α,IL-1β,S-100β protein and neuron-specific enolase (NSE) in serum were determined by enzyme-linked immunosorbent assay.The pathological changes of hippocampi were examined with a light microscope,the apoptosis in hippocampal cells was measured using TUNEL,and the apoptotic index was calculated.Results Compared with group S,the TNF-α and IL-1β levels in serum and hippocampi,levels of S-100β protein and NSE in serum and apoptotic index were significantly increased (P＜0.01),and the pathological changes of hippocampi were aggravated in I/R and P groups.Compared with group I/R,the TNF-α and IL-1β levels in serum and hippocampi,levels of S-100β protein and NSE in serum and apoptotic index were significantly decreased (P＜0.05),and the pathological changes of hippocampi were attenuated in group P.Conclusion Propofol reduces brain injury induced by hepatic I/R,and the mechanism may be related to inhibition of systemic and central inflammatory responses of preadolescent mice.

Objective To investigate the value of prenatal ultrasound in prognosis assessment of congenital diaphragmatic hernia.Methods The ultrasonographic features of 65 fetuses with congenital diaphragmatic hernia were analyzed,which were confirmed by after birth surgery or examination.The lung-to-head ratio (LHR) of unaffected side and O/E LHR (LHR compared to normal fetuses on same gestational weeks) were obtained,and then the relationship with the prognosis of neonates were analyzed.Results In 65 cases,45 fetuses survived and 8 fetuses died after surgery,while 12 cases did not undergo surgery and death promptly.Overall mortality was 30.77％ (20/65).In 12 hepatic intrathoracic type of diaphragmatic hernia cases,the mortality rate was 66.67 ％ (8/12).In 53 hepatic intra-abdominal type of diaphragmatic hernia cases,the mortality rate was 22.64 ％ (12/53).In 9 cases combined with other structural abnormalities,there were 8 cases were dead and 6 cases (6/8) with abnormal chest structure.LHR values were from 0.40 to 2.72,the average value was 1.59±0.69.It showed statistical difference on the mortality rate in fetus of congenital diaphragmatic hernia with different LHR (x2 =19.360,P＜0.001),The mortality rate in fetal of congenital diaphragmatic hernia with LHR 1.0 or less was higher than that with LHR ＞1.0.O/E LHR measurement values were from 23％ to 90％ and the average value was (58.25±17.61) ％.It showed statistical difference on the mortality rate in fetus of congenital diaphragmatic hernia with different O/E LHR (x2 15.261,P=0.002).The mortality rate in fetal of congenital diaphragmatic hernia with O/E LHR ≤45 ％ was higher than that with O/E LHR＞45 ％.Conclusion The prenatal ultrasound can be used to diagnose congenital diaphragmatic hernia,and to assess the development of unaffected lung and prognosis.