Objective To screen the amyloid protein-β(Aβ)degradation-associated genes through peripheral blood monocytes(PBMC)-extracted gene microarray analysis in patients with Alzheimer's disease(AD).Methods PBMC were isolated from blood of elderly AD patients versus age-matched healthy individuals(control).The cDNA(mRNAs)were analyzed using gene microarray.And real-time quantitative polymerase chain reaction detection and enzyme activity analysis were used to verify the primary outcome of gene chip.Results The expression of cathepsin D mRNA in peripheral blood monocytes was 104.70±15.96 in AD patients as compared with the control group 49.86±5.19,and the activity of cathepsin D was (22 620 ± 1 389) RFU in AD versus (32 210 ± 2 284) RFU in control (both P＜0.05).Conclusions The results suggest that the decreased levels of cathepsin D could be the stage markers related to the pathophysiology of AD process.Based on the microarray data,we select cathepsin D genes for further study.

Objective To investigate the relationship of the serum bilirubin level with acute ischemic stroke (AIS), and Chinese isch-emic stroke subclassification (CISS), stroke severity and short-term outcome of AIS patients. Methods 616 patients with AIS as well as 664 patients without stroke matched with gender and age were compared and analyzed with the non-conditional Logistic regression. The AIS pa-tients were divided based on the CISS, and their bilirubin levels were compared. The AIS patients were divided into high bilirubin group and normal bilirubin group, their scores of the National Institute of Health Stroke Scale (NIHSS) as admission and discharge, and neural func-tion improvement rate were compared. Results The levels of total bilirubin (TBIL), direct bilirubin (DBIL) and indirect bilirubin (IBIL) were higher in the AIS group than in the control group (P<0.01), and the TBIL was the independent risk factors of AIS (OR=1.026, 95%CI 1.012-1.041, P<0.001). There was no significant difference of the levels of TBIL, DBIL and IBIL among the patients of CISS (P>0.05). The NIHSS score was higher in the high bilirubin group than in the normal bilirubin group as admission (P<0.05), but it was not significant as discharge (P>0.05), nor the rate of neural function improvement (P>0.05). Conclusion The serum bilirubin level elevated and correlated with the severity in the AIS patients, which might be the risk of pathogenesis and AIS. The bilirubin was not various with the CISS, and might be less involved in the short-term outcome of AIS.

Objective To investigate the risk factors of recurrent ischemic stroke, and evaluate the severity and short-term outcome. Methods From March, 2014 to March, 2015, 238 patients with recurrent ischemic stroke and 378 patients with initial ischemic stroke matched with gender and age were enrolled. The clinical data of two groups were compared and the non-conditional Logistic regression model was made to analysis the risk factors of recurrent ischemic stroke. The National Institute of Health Stroke Scale (NIHSS) score as ad-mission and discharge, and the neural function improvement rate of two groups were compared. Results The incidences of leukoarailsis (χ2=8.666), hypertension (χ2=8.189), smoking (χ2=6.973) and alcohol consumption (χ2=4.722) were higher in the recurrent group than in the pri-mary group (P<0.05). Logistic regression analysis showed that leukoarailsis (OR=1.690, 95%CI:1.198~2.384, P=0.003), hypertension (OR=1.715, 95%CI:1.135~2.592, P=0.010) and smoking (OR=1.896, 95%CI:1.233~2.915, P=0.004) were the independent risk factors of recur-rent ischemic stroke. The NIHSS scores as admission and discharge were significantly higher (t=-3.645, t=-4.675, P<0.001), and the neural function improvement rate was lower (t=2.643, P<0.01) in the recurrent group than in the primary group. Conclusion Hypertension, leuko-arailsis and smoking are independent risk factors for recurrent ischemic stroke. Recurrent ischemic stroke is more serious than initial isch-emic stroke, and the short-term neural function recovers more slowly.

Objective To explore the correlation between the serum levels of fibrinogen (FIB), C-reactive protein (CRP) and homocysteine (Hcy) with the carotid vulnerable plaque in patients with large artery atherosclerosis (LAA) stroke.Methods The patients with acute ischemic stroke (AIS) admitted to the Department of Neurology in The Second Hospital of Lanzhou University from Mar. 2014 to Feb. 2015 were collected continuously, and 273 patients with anterior circulation of LAA stroke were selected based on the TOAST classification. These patients were classified as non-plaque group (n=84), stable plaque group (n=42) and vulnerable plaque group (n=147) according to the carotid ultrasonography examination. Another 182 patients without carotid disease of non-stroke selected simultaneously from our department were regarded as controls. The 19 demographic parameters and hematological indices were compared among the four groups. The logistic regression was used to screen the independent risk factors for carotid vulnerable plaque in LAA stroke patients. The Spearman rank correlation was performed to analyze the correlation between the carotid plaque vulnerability in LAA stroke patients with all the indicators.Results The levels of FIB, CRP and Hcy in the four groups showed statistically signicantcant differences (P<0.05). The multivariate logistic regression analysis revealed that FIB (OR=1.408, 95% CI 1.028-1.927,P=0.033) was the independent risk factor for carotid vulnerable plaque in patients with LAA stroke. The Spearman correlation analysis presented a positive correlation between carotid plaque vulnerability in LAA stroke patients with FIB (r=0.292;P=0.000) and Hcy (r=0.172;P=0.000). Conclusions The serum FIB and Hcy levels may be the meaningful biomarkers to predict the vulnerable carotid plaque in patients with LAA stroke. The serum level of CRP has no obvious correlation with carotid plaque vulnerability in LAA stroke patients.

ObjectiveTo investigate the serum tumor markers level of carcinoembryonic antigen(CEA) ,cytokeratin fragment antigen21-1 (CYFRA21-1),neuron specific enolase (NSE) in patients with lung cancer, and the change after chemotherapy on them. Methods Radioimmunoassay was applied to detect the levels of CEA, CYFRA21-1 ,NSE in 45 patients with advanced NSCLC before and after chemotherapy,and the tumor markers were also detected in 20 patients with SCLC and 20 patients with benign lung diseases of control groups. ResultsThe levels of CEA, CYFRA21-1, NSE in lung cancer group before chemotherapy were much higher than benign group, but there was no difference of CYFRA21-1 between the SCLC group and benign group. The same result of NSE was found between NSCLC and benign group(P ＞0. 05). The value of NSE was lower in the patients with SCLC after chemotherapy than before(P ＜0. 01 ). The level of CYFRA21-1 was lower in squamous carcinoma than before( P ＜0. 01 ). But in the adenocarcinoma group only NSE's level was lower after chemotherapy( P ＞0. 05) ,there were no differences in CEA and CYFRA21-1 ( P ＞ 0. 05 ). ConclusionThe levels of the three tumor markers rise obviously in advanced NSCLC and decrease after chemotherapy. The differences were significant with NSE in SCLC and CYFRA21-1 in squamous cell carcinoma and CEA in adenocarcinoma. The levels of serum CEA,CYFRA21-1 and NSE could be a tumor marker in progressive lung cancer. And the decrease of the levels could be used to evaluate the chemotherapeutic response respectively in different pathologic types of lung cancer.

Background Researches showed that multifocal electroretinogram (mfERG) is able to assess the retinal function in the eyes with acute Vogt-Koyanagi-Harada ( VKH ) syndrome. But the mfERG characteristics of convalescence stage of VKH are still below clear. Objective Present study was to compare and follow up the variation process of visual acuity and mfERG in acute and recovery stages of VKH syndrome. Methods This was a clinic-based retrospective study. Visual acuity, mfERG and fundus fluorescence angiography ( FFA ) were recorded from 35 eyes of 18 acute VKH cases. The period of follow-up in recovery stage lasted about 18 months with the repetitive recording results for 4 times. Results In this study, the visual acuity range in acute stage VKH was 0. 01 to 1.0, and 91.4% (32/35 eyes) was below 0.6. Compared with normal control group, the visual acuity was significantly decreased (P＜0.01). The response densities (amplitudes) of N1 ,P1 waves of the first-order kernel were significantly lowed in all the 6 rings,and the implicit times of 1-4 rings of both waves were significantly prolonged in acute VKH eyes(P＜0. 05). The abnormalities of retinal function showed a regional difference at the posterior pole retina with the dominant change in the first ring,showing a cutting off78% in the P1 amplitude. The abnormal degree of mfERG was more serious as the the increase of retinal eccentricity. In 2 months of convalescence after glucocorticosteroids therapy,the range of visual acuity were 0. 1-1.2 ,and the amplitudes of N1, P1 of 1-2 rings were greatly elevated in comparison with acute on-set (P＜0. 05 ). However, there was still a remarkable difference in the amplitudes of from 1 through 6 rings,comparing with normal. The response density of P1 wave from whole recording region was only 44% of normal. Though the visual acuity was stable during the follow-up duration, a decreasing tendency in N1 and P1 amplitudes were seen. The implicit times of both wave shortened only in 1-3 rings in recovery stages of VKH (P＜0.05). Conclusion VKH syndrome cause serious damage of posterior retinal function.Macular region is the site with greater retinal functional lesion and restore before and after medication. This hardly recovery of retinal function can last over one and half year,even satisfied visual acuity is stable after proper treatment.

AIM: To observe the dynamic changes of interleukin-4(IL-4),IL-10,IL-12 in rat serum and lung tissues during acute respiratory distress syndrome (ARDS). METHODS: The ARDS model of rats was induced by intravenous injection of oleic acid. The levels of IL-4 ,IL-10,IL-12 in serum and the supernatant of lung tissues were measured by enzyme linked immunosorbent assay (ELISA). RESULTS: The Levels of serum and lung IL-10,IL-12 in ARDS rats were increased in 4 h ,8 h,16 h group compared with control group . The levels in IL-10 in serum in 16 h group and IL-10 in lung tissues of 8 h group were lower than that in 4 h group. The Levels of IL-4 in serum in 4 h, 8 h group were higher than that in control group , while IL-4 in 16 h group was lower than that in 8 h group. IL-4 of lung tissues in 4 h,8 h,16 h group were increased significantly,but in 16 h group were lower than that in 8 h group. The biggest changes of pulmonary coefficient and histopathology were observed at 4 h after injection of oleic acid. CONCLUSIONS: IL-4,IL-10 and IL-12 might play important roles in inflammatory reaction induced by oleic acid. The pro- and anti-inflammatory cytokines produced successively during ARDS. The relationship between unbalanced cytokines and lung injury in ARDS needs to be further studied.

Objective To detect the expression of aquaporin 1 in pancreas of rats with acute necrotizing pancreatitis (ANP) and to study the effect of Dachengqi decoction on it.MethodsOne hundred and sixty male SD rats were randomly divided into control group ( C group,n =32 ),ANP group ( n =32),Dexamethasone group (De group,n =32),Acetazolamide group (A group,n =32) and Dachengqi decoction group (DD group,n =32).ANP model was induced by retrograde injection of 5％ sodium taurocholate into the biliary and pancreatic duct.Rats in De group received dexamethasone (4 mg/kg) intravenously after ANP induction; while rats in A group received 1 ml acetazolamide via gastric lavage 2 h before ANP induction; rats in DD group received 2 ml Dachengqi decoction via gastric lavage 48,24,2h before ANP induction; rats in C group received laparotomy.Eight rats in each group were sacrificed at 3 h,6 h,12 h and 18h after induction of ANP models.Quantity of ascites and levels of serum amylases were measured.Pathological changes in pancreas tissue were detected by HE and electron microscope.Capillary permeability in pancreas tissue was detected by Evans Blue (EB) extravasations method.AQP1 expression in pancreas tissue was detected by real-time PCR and Western blotting.ResultsLevels of serum amylase in ANP group was significantly higher,and the pancreatic injuries were obvious ; the levels of serum amylase in De group and DD group was lower than that in ANP group,and the pancreatic injuries were attenuated.The levels of serum amylase in A group were higher than that in ANP group,and the pancreatic.injuries were more severe than that in ANP group.Six hours after ANP induction,the levels of EB in pancreas were (13.44 ±2.56),(126.35 ± 14.80),(86.31 ± 14.46),( 108.99 ± 15.07 ),(78.29 ± 16.85 ) mg/L In C group,ANP group,De group,A group and DD group,and the expression of AQP1 mRNA in pancreatic tissue was ( 170.07 ± 22.48 ) ％,( 83.93 ± 8.98 ) ％,( 117.09 ±10.70 ) ％,( 69.00 ± 8.98 ) ％,( 112.82 ± 11.79 ) ％ ; and the expression of AQP1 protein was 0.23 ± 0.06,0.10 ±0.02,0.32 ±0.03,0.13 ±0.02,0.45 ±0.04.The content of EB in ANP group was higher than that in C group,while the expression of AQP1 mRNA and protein in ANP group was significantly lower than that in C group (P ＜ 0.05 ).The content of EB in De group and DD group was significantly lower than that in ANP group,while the expression of AQP1 mRNA and protein was significantly higher than that in ANP group (P ＜ 0.05).ConclusionsAQP1 plays an important role in the pathogenesis of capillary endothelial barrier dysfunction in rats with ANP.Dachengqi Decoction can attenuate pancreatic injuries of rats by regulating the expression of AQP1.

Mounting evidence has shown that side population (SP) cells are enriched for cancer stem cells (CSCs) responsible for cancer malignancy. In this study, SP technology was used to isolate a small subpopulation of SP cells in human gallbladder cancer cell line GBC-SD, and SP cells which had superior potential for proliferation in vitro and tumorigenesis in vivo were identified. Importantly, the abundance of GBC-SD SP cells was increased by a transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT), and this effect was accompanied with a strong up-regulation of ABCG2 mRNA expression, and a decreased sensitivity to mitoxantrone. SP cells were restored upon the removal of TGF-β and the reversion of the cells to an epithelial phenotype, and smad3-specific siRNA reduced SP abundance in response to TGF-β. In conclusion, TGF-β-induced EMT by smad-dependent signaling pathway promotes cancer development and anti-cancer drug resistant phenotype by augmenting the abundance of GBC-SD SP cells, and a better understanding of mechanisms involved in TGF-β-induced EMT may provide a novel strategy for preventing cancer progression.

Objective To explore early diagnosis and treatment of congenital esophageal atresia and tracheoesophageal fistula.Methods Clinical data of 11 patients with congenital esophageal atresia and tracheoesophageal fistula were analyzed retrospectively.Definite diagnoses were made for all cases in 24 hours through making an esophagus opacification with acetrezoic acid or iodinated oil.And an esophagus anastomosis outside pleura was made.Some experience of diagnosis and therapy were summarized.Results All of the 11 cases underwent operation.Among them,9 cases were cured (81.8%),and 2 cases died(18.2%).Anastomosis stenosis of esophagus was found in 1 case after operation,which was cured through esophagus dilatation.Tracheoesophageal fistula was found in another case after operation and it was cured through combined treatment including anti-infection, nutritional support and sufficient draining.Conclusion Early diagnosis and surgical treatment, postoperative care,prevention and cure of complication are very important to improve the survival rate of the patients with congenital esophageal atresia and tracheoesophageal fistula.