Heme oxygenase-1(HO-1) is an inducible stress protein.In addition to its role in heme degradation,several positive biological effects exerted by this enzyme have highlighted in recent years as anti-inflammatory,anti-apoptotic,anti-proliferative and cytoprotective functions.This oxidase system with multiple functions takes part in the pathophysiology of cardiovascular system.It is related to a variety of cardiovascular diseases including hypertension,atherosclerosis,ischemia/reperfusion injury and postangioplasty restenosis.

Objective To explore the neuroprotective effect and mechanism of picroside II on ERK1/2 signal transduction pathway after cerebral ischemia injury in rats.Methods The focal cerebral is-chemic models were established by inserting a monofilament threads into middle cerebral artery occlusion (MCAO) in 100 Wistar rats and treated by injecting picroside II (20 mg/kg) intraperitoneally.The neu-robehavioral function was evaluated by modified neurological severity score points ( mNSS) test.The cerebral infarct volume was measured by tetrazolium chloride ( TTC) staining.The apoptotic cells were counted by terminal deoxynucleotidyl transferase dUTP nick end labeling ( TUNEL) assay.The expression of pERK1/2 in cortex was determined by the immunohistochemistry ( IHC) and Western Blot ( WB) .Results mNSS test showed that severe neurological dysfunction was found in model and LPS groups,and the scores of mNSS were significantly increased;meanwhile the scores of mNSS in treatment group and U0126 group were signifi-cantly lower than that in model and LPS groups (P<0.05).TUNEL assay showed that the apoptotic cell inde-xes (ACI) in different groups were (0.06±0.02),(0.27±0.03),(0.07±0.02),(0.26±0.03)and(0.09± 0.05) ,and the ACI in treatment and U0126 groups was obviously lower than that in model and LPS groups (P<0.05) .With IHC and WB,pERK1/2 level in model group was the highest,which was slightly higher than that of LPS group,and pERK1/2 expression in treatment and U0126 groups was significantly decreased com-pared with that in model and LPS groups (P<0.05) .Conclusion The activation of ERK1/2 by cerebral is-chemia could induce the cell apoptosis.Picroside II might reduce cell apoptosis by inhibiting the activation of ERK1/2 in ischemic brain injury.

Objective To investigate the disinfection effect of the endoscope disinfection machine with acidic oxidizing poten‐tial water on the fiber bronchoscopy .Methods Totlly 460 cases of contamination after diagnosis and treatment in the department , were randomly divided into experimental group (using electrolyzed oxidizing water as disinfectant ;according to the cleaning and dis‐infection of endoscope Koeman brand ECM‐03A type machine bronchoscope disinfection) and control group (with 2% glutaralde‐hyde disinfectant of the traditional five tank cleaning disinfection method ) ,evaluation of endoscopic surface cleanliness ,surface at‐tachment ,pipe blockage and bacterial colony detection .Results The experimental group was better than the control group in the aspects of endoscopic surface cleanliness ,mirror surface attachment ,pipe blockage and so on ;The number of sterile growth in the experimental group was higher than that in the control group ,both in the inner cavity sampling method and the outside sampling method .The number of cases of ≥20 CFU/piece in the experimental group was significantly less than that in the control group , with the cavity sampling method ,the qualified rate of the experimental group was also significantly higher than that of the control group ,the difference was statistically significant (P< 0 .05) .Conclusion The application of acidic oxidizing potential water as a disinfectant in the whole automatic endoscope disinfection machine significantly improve the quality of cleaning and disinfection ,at the same time ,and reduce human labor strength ,improve the application efficiency of fiber bronchoscopy ,worthy of promotion .

Objective To detect the expression levels of serum alpha fetal protein (AFP),carbohydrate antigen 199(CA-199) and carcinoembryonic antigen(CEA) in a rat model of liver cancer and elderly liver cancer patients,and explore its clinical significance.Methods A rat model of liver cancer was successfully established by intraperitoneal injection of a low dose of diethylnitrosamine (DEN).The expression levels of serum AFP,CA-199 and CEA in rats were determined and compared during the development of liver cancer.Blood samples were collected from elderly subjects with normal liver and elderly liver cancer patients(n=80,each).The expressions of serum AFP,CA-199 and CEA were determined and compared between healthy elderly patients and elderly liver cancer patients.Results Serum levels of AFP,CA-199 and CEA were higher in liver cancer rats than in normal rats [(4.21±1.32) μg/Lvs.(1.05±0.33) μg/L,(3.78±1.04) kU/L vs.(1.00±0.28) kU/L,(3.54±0.92) μg/Lvs.(1.10±0.37) μg/L,t=9.493,8.609,7.675,respectively,all P=0.000].Serum AFP,CA-199 and CEA levels were higher in elderly patients with liver cancer than in elderly subjects with normal liver [(66.89±9.33) μg/L vs.(2.56±1.09) μg/L,(116.89±43.33) kU/L vs.(5.56±1.26) kU/L,(5.83 ± 1.56) μg/L vs.(1.17 ± 0.51) μg/L(t=14.379,17.470,10.677,respectively,all P=0.000).The positive rate of joint detection of AFP,CA-199 and CEA was higher in elderly patients with liver cancer than in elderly subjects with normal liver [77.50％ (62/80) vs.1.25％(1/80),x2 =17.260,P=0.000].Conclusions The joint detection of AFP,CA-199 and CEA can help increase the diagnostic rate of liver cancer in elderly patients.

[Summary] To investigate the difference in serum pigment epithelium-derived factor ( PEDF) among type 2 diabetic patients before and after use of dipeptidyl peptidase-4 inhibitors linagliptin for treatment, and to explore the correlation of serum PEDF with lipids, body mass index, and HbA1C . 39 patients with recently diagnosed type 2 diabetes and 30 healthy individuals were enrolled. Baseline weight, waist circumference, body mass index, fasting plasma glucose, HbA1C , serum glutamic-pyruvic transaminase, glutamic oxaloacetic transaminase, total cholesterol, triglyceride, high density lipoprotein-cholesterol, low density lipoprotein-cholesterol ( LDL-C) , and PEDF measured by enzyme linked immunosorbant assay were determined both in the diabetic and control subject. The treatment group was treated with oral linagliptin 5 mg/d for six month, serum PEDF and clinical parameters were determined in the diabetic group during 6 months of treatment. ( 1 ) PEDF levels were found to be comparable with the controls ( P=0. 584);LDL-C and waist circumference showed positive correlation with PEDF(P<0. 05 or P<0. 01). (2) PEDF level was significantly increased in patients with type 2 diabetes after linagliptin treatment [(3. 21 ± 1. 91 vs 2. 45 ± 1.53)μg/ml,P<0.01]. SerumPEDFlevelinpatientswithtype2diabeteswassimilartothatofhealthycontrolswith associated LDL-C and waist circumference. After linagliptin treatment, serum PEDF level was raised, suggesting that it may have certain protective effect for diabetic vascular complications.

Objective To investigate the expressions of insulin-like growth factor receptor-1 (IGF-1R) and insulin-like growth factor binding protein-3 (1GFBP-3) and their correlations with clinicopathological parameters in the primary colon cancer,as well as their roles in lymph node metastasis of colon cancer.Methods The expressions of IGF-1R and IGFBP-3 in 78 cases of colon cancer tissues and 78 cases of normal colon mucosa tissues were detected by SP immunohistochemical technology and the correlations between the expressions and the clinical pathological parameters of colon cancer were analyzed.Results The positive rate of IGF-1R in colon cancer (66.7％,52/78) was significantly higher than that in control group (24.4％,19/78),x2 =28.150,P =0.000.The positive rate of IGFBP-3 in colon cancer (73.1％,57/78) was significantly lower than that in control group (89.7％,70/78),x2 =7.158,P =0.007.IGF-1R expression in colon cancer was significantly correlated with the invasion (x2 =5.804,P =0.016),TNM stage (x2 =5.246,P =0.022) and lymph node metastasis (x2 =12.955,P =0.000).IGFBP-3 expression in colon cancer was signi-ficantly correlated with the TNM stage (x2 =7.096,P=0.008),lymph node metastasis (x2 =5.893,P =0.015) and distant metastasis (P =0.003).Both with other factors had no significant correlation (P ＞ 0.05).1GF-1R expression and IGFBP-3 expression showed a negative correlation (r =-0.245,P =0.03).Conclusion The over expression of IGF-1R and low expression of IGFBP-3 are associated with TNM stage and lymph node metastasis in colon cancer.IGF-1R and IGFBP-3 may become new targets of the treatment of colon cancer.

BACKGROUND:Although there is no report of adipose-derived stem cells in ureteral repair, but with the deepening of the research of adipose stem cells, the differentiation conditions of adipose-derived stem cells to the vascular endothelial cells, smooth muscle cells and urothelial cells are more mature, and the experimental research of adipose-derived stem cells in the repair and reconstruction of kidney and bladder is also increasing.
OBJECTIVE:To summarize the adipose-derived stem cells research and its application in damage and repair of urinary system in recent years.
METHODS:The first author retrieved PubMed database and CNKI databases for articles relevant to adipose-derived stem cells in the repair of urinary system published between January 2001 to September 2013 using the keywords of“adipose tissue-derived stem cel/adipose tissue-derived stromal cells/ADSCs;tissue engineering;kidney;ureter;ureathra;bladder;urology”in English and Chinese, respectively. Final y, 52 articles were included for further analysis.
RESULTS AND CONCLUSION:Adipose-derived stem cells which can be found easily and have the unique advantages of multi-directional differentiation ability have been used for repairing and constructing the urinary system. Adipose-derived stem cells provide a new model of treatment for the urinary tract, which solves the traditional problems, including immune rejection, source of organs and ethical issues, and become an ideal cellsource in repair of urinary system. Accumulated data related to adipose-derived stem cells and its experiment and clinical application in repair of urinary system injuries have been reported. But before the cells are widely used in clinic, the fol owing problems need to be solved:its specific surface marker identification, specific conditions and control of celldifferentiation, mechanisms of action.

Objective To observe the effect of exenatide on endoplasmic reticulum stress (ERS) in human renal mesangial cells (HRMCs) injured by fluctuating hyperglycemia culture,and to explore the mechanism.Methods HRMCs were randomly divided into three groups:control group (group N,cells were cultured in 5.6 mmol/L glucose for 24 h),fluctuating hyperglycemia group (group F,cells were cultured in 30 mmol/L glucose for 3 h,5.6 mmol/L glucose for 2 h,repeated three times in one day,then 5.6 mmoll/L glucose overnight),fluctuating hyperglycemia and exenatide group (group F+G,HRMCs were cultured in fluctuating hyperglycemia and 100 nmol/L exenatide).MTT assay was used to measure the viability in each group.The apoptosis rates were detected by flow cytometry in three groups.The relative expression of glucose regulated protein78 (GRP78) and CCAAT/enhancerbinding protein homologous protein (CHOP) were tested by Western blot assay.Results Compared with the group N,the cell proliferation level decreased,the cell apoptosis rate increased,and the expression levels of GRP78 and CHOP increased in F group (P ＜ 0.05).After treatment with exenatide,the cell proliferation rate increased,cell apoptosis rate decreased (P ＜ 0.05),and the expression levels of GRP78 and CHOP decreased in F+G group,compared with those of the group F (P ＜ 0.05).Conclusion Exenatide can reduce the damage of fluctuating hyperglycemia on HRMCs by down-regulating the stress levels of the endoplasmic reticulum stress.

Objective To study the relationship between high on-treatment platelet reactivity (HTPR) and early neurological deterioration (END) in acute non-cardiogenic cerebral infarction patients.Methods Two hundred and fifteen acute non-cardiogenic cerebral infarction patients were divided into END group (n=55) and EDD-free group (n=160).The patients were given oral aspirin (300 mg daily) on the day after admission,and fasting blood samples were taken at 6-24 h after the first dose of aspirin.Their platelet aggregative function (PAGT) was assayed with ADP to detect the platelet responsiveness to aspirin.The incidence of HTPR was compared between the two groups.The independent risk factors for END were analyzed by multivariate logistic regression analysis.The value of PAGT in predicting END was assessed according to its ROC curve.Results The incidence of HTRP was higher in END group than in END-free group (63.34％ vs 43.75％,P＜0.05).Multivariate logistic regression analysis showed that HTRP was an independent risk factor for acute non-cardiogenic cerebral infarction.The area under the ROC curve was 0.864 for PAGT in predicting acute non-cardiogenic cerebral infarction (95 ％ CI:0.806-0.922,P=0.000).Conclusion HTPR is closely related with END in acute non-cardiogenic cerebral infarction patients.

Objective To investigate the effect of advanced oxidation protein products (AOPPs) on human renal tubular epithelial cells(HK-2) autophagy.Methods HK-2 cells were stimulated with AOPPs.RT-qPCR and Western blot were used to determine the expression of autophagy related protein LC3-Ⅱ/LC3-Ⅰ,Beclin1 and p62;Western blot was utilized to examine the activation of p38 MAPK pathway.Then p38 MAPK inhibitor (SB203580) was added and co-processed with AOPPs.The change of autophagy was observed Also,autophagy inducer rapamycin was added and co-processed with AOPPs.RT-qPCR and Western blot were used to detect the expression of cell cycle inhibitory protein p27.The cell total protein level was detected by the bicinchoninic acid (BCA) method.The hypertrophy change was observed.Results AOPPs down-regulated the expression of LC3-Ⅱ/LC3-Ⅰ and Beclin1,up-regulated expression of p62 and activated p38 MAPK pathway;in comparison with the AOPPs alone treatment group,the expression of LC3-Ⅱ/LC3-Ⅰ and Beclin in the SB203580 co-processing group was increased,while p62 was decreased;the p27 expression and cells total protein in the sirolimus co-processing group were down-regulated.Conclusion AOPPs inhibits the autophagy of HK-2 cells by activating p38 MAPK pathway and the autophagy inhibition participates in HK-2 cell hypertrophy.