Objective To investigate the changes of plasma fibrinolytic activity and D dimer level in the primary hypertension of the elderly.Methods ELISA was applied to measure blood and urine D dimer.Chromophore substrate method was used to detect PL,Plg,t PA and PAI 1.Results The levels of PAI 1,D dimer and Plg were obviously higher in the elderly primary hypertension and hypertentive kidney disease than those in the control group,while t PA and PL activity were lower than in the control group.Conclusion The changes of PLA and D dimer play an important role in hypertension and hypertentive renal disease of the elderly,on which the early diagnosis can be based.

Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt.

Objective To explore the role of Hippo pathway in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD),and find potential targets for drug therapy.Methods By means of immunofluorescence staining,Western blotting,Real-time PCR,the differences of sublocalization,expression and phosphorylation level about Hippo pathway molecules in Han:SPRD (cy/+) and ADPKD patients compared with the control were observed.Knockdown Yes kinaseassociated protein (YAP),transcriptional coactivator with PDZ binding motif (TAZ) and large tumor suppressor kinase1 (LATS1) in cystic lining epithelium cell line WT9-12 were took by siRNA interference,and then their effects on cell proliferation,apoptosis and cell cycle were assessed.Results In cystic lining epithelium of Han:SPRD(cy/+),decreased expression of LATS1 and increased expression of YAP were found compared with the control,and the immunofluorescence of YAP was distributed both in cytoplasm and nucleus,while distribution and expression level of TAZ were without significant variance.Abnormal mRNA expressions of Hippo pathway components in ADPKD patients were found (P ＜ 0.05).Down-regulation of LATS1 in WT9-12 cells could prohibit phosphorylation of YAP,and prompted proliferation and cell division.Knockdown YAP in WT9-12 cells could inhibited cell proliferation by arresting cell cycle in G0/G1 phase,but down-regulating TAZ showed no significant differences in proliferation and cell cycle.Conclusions Altered Hippo signaling exists in ADPKD,and YAP activation may be one leading cause of autosomal dominant polycystic kidney disease onset.In vitro,knockdown YAP in WT9-12 cells can inhibit cell proliferation by arresting cell cycle and depressing cell division,suggesting the expression level and activity of YAP are potential targets for ADPKD treatment.

Objective To investigate the differences between animal temperature controller (ATC) and artificial climate chamber (ACC) used for the establishment of classical heat stroke (CHS) rat model.Methods Twenty-four male specific pathogen-free Wistar rats were randomly (random number) and equally assigned to three groups,namely room temperature control (C-C) group,heat stroke under conscious state (HS-C) group,and heat stroke under anesthesia (HS-A) group.Rats of HS-C or HS-A group were placed into ACC or ATC,then exposed to 35 ℃ heat stress.The systolic blood pressure (SBP) and core body temperature (Tc) were monitored.The time required for onset of HS was recorded.The white blood cell count (WBC) in peripheral blood and serum levels of C-reactive protein (CRP),tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) were measured.The histopathological changes of major organs were also confirmed by hematoxylin-eosin (HE) staining.Results The onset time in HS-A group was significantly shorter thanthatin HS-C group [(40.0 ± 4.3) minvs.(110.1 ± 5.3) min,P＜0.01].The SBP and Tc at this moment were lower in HS-A group [(159.1 ± 5.91) mmHg vs.(174.54 ± 5.77) mmHg,P＜0.01;(43.5 ± 0.4)℃ vs.(44.4 ± 0.2)℃,P＜0.01].TheWBC,CRP,TNF-α and IL-1 β levels of these two HS groups were dramatically elevated compared with C-C group (P ＜0.01).The inflammatory cytokines levels in HS-A group were significantly lower than those in HS-C group (P ＜ 0.01),but there was no difference in WBC between them (P ＞ 0.05).However,there was no obvious difference in histopathological change in major organ observed between HS-A and HS-C groups.Conclusions In comparison of these two methods,ATC is similar to ACC in respect of the establishment of CHS rat model.ATC is quicker in onset of HS,and more simplified and economical than ACC and could substitute ACC.

Objective To investigate the effects of a novel PPARγ agonist DH9 on Wntβ-catenin pathway in human polycystic kidney cystic-lining epithelial cells (WT9-12).Methods WT9-12 cells were treated with different concentrations of DH9 for 72 hours and the proliferation was assessed by MTT.WT9-12 cells were pretreated with SB216763 or GW9662 for two hours and then treated with DH9 for 72 hours.Western blotting was applied to detect the protein expression of β-catenin,phospho-β-catenin,GSK3β,phospho-GSK3β.Results DH9 could effectively inhibit the proliferation of the cells.60 μmol/L DH9 could facilitate β-catenin down-regulation (P＜0.01) and phospho-β-catenin up-regulation (P＜0.01).Inhibition of GSK3β by SB216763 could protect WT9-12 cells against DH9-facilitated β-catenin repression in a dose-dependent manner despite phosphorylating deactivation,but PPARγ inhibitor GW9662 couldn't.Conclusions DH9can effectively block the proliferation of WT9-12 cells.The effect may be mediated by facilitating the down-regulation of β-catenin via GSK3β-dependent mechanism.

Objective To observe the impact of heparanase on glomerular endothelium glycocalyx during sepsis and to investigate the prevention of glycocalyx injury.Methods C57/BL6 mice were injected with lipopolysaccharide (LPS) or tumor necrosis factor-α(TNF-o) and sacrificed one hour later.Glomerular endothelium glycocalyx traced with lanthanum was observed by transmission electron microscope(TEM).Western blotting was used to observe heparanse protein expression of renal cortex tissue.Human renal glomerular endothelial cells (HRGECs) were stimulated with TNF-α and active heparanase protien expression was detected by Western blotting.Mice were administrated with heparin sodium or heparinase Ⅲ and renal endothelium glycocalyx was observed by TEM.Urine during twenty-four hours was collected to measure urinary albumin and creatinine.The ratio of albumin to creatinine was calculated and compared among groups.Results The glomerular endothelium glycocalyx of LPS group and TNF-α group was degradated and the one of podocyte was integrated.Renal cortex tissue heparanase protein expression was significantly increased since one hour after LPS injection (P ＜ 0.01).The protein expression of activited heparanase of HRGECs which were stimulated with TNF-α was increased (P ＜ 0.05).Administration of heparin sodium which could inhibit the activity of heparanase could prevent the glycocalyx form degradation.The ratio of urine albumin to creatinine of heparin sodium group was decreased compared with LPS group (P ＜ 0.05) and the ratio of heparinase Ⅲ group was higher than control group(P ＜ 0.01) as a result of degradation of glomerular endothelium glycocalyx.Conclusions During the early stage of sepsis,TNF-α can induce glomerular endothelium heparanase to increase and active,and consequently the glycocalyx is degradated which leads to albuminuria.Inhibition of heparanase can protect glomerular endothelium glycocalyx and prevent albuminuria.

Objective To study the diagnostic significance and clinical value of genetic analysis in children with neonatal diabetes. Methods Gene mutation analysis was performed in four patients from Zhengzhou children ' s hospital with diagnosis of with neonatal diabetes. Therapeutic effect of glibenclamide in patients with or without gene mutation was compared. Results KCNJ11 gene mutation was found in two patients with neonatal diabetes. Glibenclamide was found only effective for blood glucose control in patients with KCNJ11 mutation. Therefore, Insulin remains the best therapeutic choice in patients without the genetic mutation. Conclusions Genetic mutation status may be useful in choosing treatment options of neonatal diabetic patients, therefore, should be performed in all children with neonatal diabetes.

Objectives To investigate preparation of gemcitabine albumin nanoparticles, and its property of slow-release, the cytotoxic effect on pancreatic cancer cells (PANC1) in vitro, for improving the effect of regional intra-arterial infusion chemotherapy in pancreatic cancer with new medicament in the future. Methods The gemcitabine albumin nanoparticles were prepared with bovine serum albumin and gemcitabine with the desolvation-crosslink method, the concentration of gemcitabine was detected by high performance liquid chromatography (HPLC). The cytotoxic effect on pancreatic cancer cells in vitro were detected with MTT colorimetric assay. Results The mean diameter of gemcitabine albumin nanoparticles was (156.2±2.2) nm, and Zeta potential was (-20.4±1.41)mV, drug loading was 10.8%, drug release time in virto was 3 hours respectively. Gemcitabine albumin nanoparticles (0.01～50 μg/ml) had a 31%～44% inhibitory rate on PANC1 cell, which was similar to the inhibitory rate of same concentration of gemcitabine (26%～47%). Conclusions The new preparation of gemcitabine albumin nanoparticles had obvious drug slow-release effect, which may help improve the effect of regional intra-arterial infusion chemotherapy for pancreatic cancer.

Objective To investigate the awareness of osteoporosis and its influential factors in middle-aged and older people. Methods By using self-designed questionnaire, 354 middle-aged and old people were investigated as to their awarness of osteoporosis in Chajiao street community in Guangzhou. Among them, 58 people were measured the bone density in the calcaneal bone by Ultrasound. Results The average score of the questionnaire was 9.46 ± 5.13, and the accuracy was 39.4%. In the diagnosis and treatment, the accuracy was just 17.8%. The diet (the accuracy in 54%) and sport (the accuracy in 50.3%) were good. The statistical analyses showed the linear relationship between the T value of bone density and the age (P = 0.021), between the T value and the score (P = 0.047). Wilcoxon rank sum test found that the T value between female and male was significantly different (Z = -3.749, P < 0.000). With multiple linear regression analysis, the T value had a linear correlation with the score (F = 4.224, P = 0.045) positively. Conclusions Currently, the awareness of osteoporosis in the middle-aged and old people was inadequate. To better prevent osteoporosis, the propogation of knowledge and guidance provided by clinicians in osteoporosis should be improved necessarily and emergently.

Objective To investigate healthcare-associated infection(HAI)in patients in a cancer hospital,provide reference for controlling HAI in cancer patients,and guide rational use of antimicrobial agents.Methods Clinical data of patients in a cancer hospital between August 2006 and July 2012 were analyzed retrospectively.Results The incidence of HAI case was 1 .53% (2 060/134 389),and annual incidence showed a downward trend.The main in-fection site was lower respiratory tract (46.46%,n=957),followed by bloodstream (15.63%,n=322),abdominal and pelvic (14.03%,n=289).The main pathogens were Pseudomonas aeruginosa (16.16%,n=350),Staphylo-coccus aureus (9.97%,n=216),Klebsiella pneumoniae (9.79%,n=212),Escherichia coli (9.65%,n=209), and Candida albicans (6.51 %,n=141 ).Gram-negative bacilli,including Klebsiella pneumoniae and Escherichia coli ,were sensitive to carbapenems and β-lactamase inhibitors.Conclusion Lower respiratory tract is the major HAI site in patients with cancer,and gram-negative bacteria are the main pathogens.Carbapenems andβ-lactamase inhibitors are recommended for the empirical treatment of HAI in cancer patients.