Objective To explore the effect of two methods on phlebitis induced by peripherally intravenously infused dopamine. Methods One hundred and ninety-five patients with phlebitis caused by peripherally intravenously infused dopamine were randomly divided into experiment group and control group according to the parity of hospitalization number in our department during September 2013 to December 2014. Ninety-eighty cases were assigned in the experiment group and 97 in the control group. In the control group, the venous infusion was done with 24G common intravenous detaining needle and general micro pump infusion extension tube. In the experiment group, it was done with 24G safety intravenous detaining needle, disposable connecting pipe with precision filter and DuoDERM attached to the needle wing of puncture site and its upper skin. The two groups were compared in terms of the incidence and occurrence time of phlebitis. Results The incidence of phlebitis in the experiment group was significantly lower than that of the control group, and its severity significantly lower than that of the control group. In addition, the occurrence time was significantly longer than that in the control group. Conclusion Venous infusing with 24G safety intravenous detaining needle, disposable connecting pipe with precision filter, and DuoDERM attached to the needle wing of puncture site and its upper skin can effectively reduce the incidence and occurrence time of phlebitis caused by dopamine.

Exosomes are vesicles of endocytic origin released from different cell types under both normal and pathological conditions.Proteomics is an emerging discipline for studying composition and mechanics and interac-tion of proteins with regard to disease occurrence、cellular metabolism,etc.Progress of research on exosomes from tumor cell at proteomics technology platforms in aspect of clarifying mechanisms of shaping and sustaining micro-enviroment of tumor growth and survival and metastasis, induce tumor proliferation, Immunosuppressive effects or immune evasion, and discovering biomarker, makes a promising prospect of exsomes in clinical diagnosis and treatment.

AIM:To study the potential pathological role of abnormal expression of endogenous angiopoietins in progressive glomerulosclerosis.METHODS:80 male Wistar rats were randomly allocated into sham operation group(sham,n=25),unilateral nephrectomy group(UNx,n=25)and UNx+daunorubicin(DRB)group(n=30).The rats in DRB group were intravenously injected with DRB(5 mg/kg)on the seventh and the fourteenth day respectively after excising one kidney.Then,at week 1,2,4,6 and 8,5,male Wistar rats from each group were taken randomly for determining 24 h urinary protein quantitative measurement(24hUPQ),BUN,Scr,and the kidneys were examined by electronic microscope,PAS staining,immunohistochemical staining and in situ hybridization histochemistry.RESULTS:There was a trend towards an increase respectively in levels of 24hUPQ,Bun,Scr,GSI in DRB from week 2 to week 8.Electronic microscope revealed that podocyte injury presented in DRB group.Expression of Ang1 mRNA and protein in glomerulus in DRB group decreased,while expression of Ang2 protein in glomeruli in DRB group increased.In DRB group,expression of Ang1 protein had a negative correlation with 24hUPQ,BUN,Scr,GSI,expression of Ang2 protein and CoIV protein.Expression of Ang2 protein had a positive correlation with 24hUPQ,BUN,Scr,GSI,expression of CoIV protein.CONCLUSION:Podocyte injury may lead to glomeruli abnormally express angiopoietins.A decrease in expression of Ang1,and upregulation in expression of Ang2 may facilitate progressive glomerulosclerosis in the rat.

AIM: To establish a model of subtotal nephrectomy (SNx) and investigate the changes of apoptosis and apoptosis-related genes (Bax, bcl-2, caspase-3, caspase-8 and caspase-9) in the rat remnant kidney. METHODS: Remnant kidneys were produced in adult male SD rats by 5/6 nephrectomy. The renal function and histopathological changes were evaluated at 1, 2, 4, 8, 12, 16, 26 and 40 weeks after operation. The tissues of remnant kidneys were collected to detect apoptosis cells by in situ end-labeling of cleaved DNA (TUNEL) and proliferating cells by determining the proliferating cell nuclear antigen (PCNA). The expression of Bax, bcl-2, caspase-3, caspase-8 and caspase-9 was measured by RT-PCR and Western blotting. The proteins were detected by immunohistochemistry staining. The relation between apoptosis, proliferation, glomerulosclerosis and renal interstitial fibrosis was also observed. RESULTS: The results showed the renal pathological dynamic changes in 5/6 nephrectomy remnant kidneys were tubule-interstitial inflammation and fibrosis, as well as glomerulosclerosis. There were transient increases in both proliferating and apoptotic processes in glomerulus, tubules and interstitium. Apoptosis was increased and most of apoptotic cells were detected in tubular epithelial cells and interstitial area. The mRNA and protein expression of Bax, caspase-3, caspase-8 and caspase-9 were increased in all course, and peaked at week 4 and 40 in the SNX rats. The successive changes of these parameters were parallel to the level of focal inflammation in interstitium. Glomerulosclerosis index was related with focal inflammation cells and 24 hours urine protein (r=0.788, 0.822; P

Objective To investigate the regulatory effect of adrenomedullin (AM) on the cell-cell contact formation of podocytes and the possible mechanism.Methods Podocytes were treated with AM (10-7 mol/L),AM combined with a PKA inhibitor H89 (10-4 mol/L),and forskolin (10-5 mol/L) as positive control respectively for 12 hours.Immunofluorescent staining was applied to observe the distribution of cell adhesion molecules and actin-associated proteins.Western blotting assay was used to assess their protein levels.Rho GTPases activity was analyzed by GST-pull down assay and their protein levels were tested by Western blotting.Results AM induced the redistribution of adhesion molecules,actin-associated proteins as well as the F-actin at cell-cell contacts between podocytes.This effect was similar to that of forskolin and could be blocked by H89.The levels of those proteins did not change significantly (P ＞ 0.05).AM up-regulated the activities of RhoA,Rac1 and Cdc42 (P ＜ 0.05),which were partially blocked by H89.The protein levels of Rho GTPases showed no difference compared with the control (P ＞ 0.05).Conclusions AM may promote cell-cell contact formation of podocytes,probably through enhancing the activity of Rho GTPases and then resulting in the redistribution of adhesion molecules,actin-associated proteins and F-actin,which is partially mediated through cAMP-PKA signaling pathway.

Objective To investigate the influence of ursolic acid on vascular endothelial growth factor ( VEGF) , cycloxygen-ase-2 (COX-2), and matrix metalloproteinases-2 (MMP-2) expressed in the mouse retinal ischemic model , and to explore the mecha-nisms of anti-angiogenesis.Methods Sixty 7-day clean-class C57BL/6J mice were divided randomly into 6 groups [ n =10 mice (20 eyes) per group]:blank control, model control (PBS), positive control (triamcinolone), and ursolic acid (UA) intervention (low-dose, medium-dose, and high-dose).Mice in the blank control group were raised in air , and mice in other groups in(75%±2%)O2 high-oxygen environment for 5 consecutive days .Mice in the model control group and breastfeeding mice were put back in air environ-ment (21%O2 ) on the 12th day after the new-born mice to induce the generation of retinal neovascularization .When models were suc-cessful, the drug treatments were applied immediately to the corresponding groups , with injection of 3μl of sterile PBS in model control group, 3 μl of 1.5, 3.00 and 6.0 μg UA in UA intervention group, and 3 μl of triamcinolone (1 ml∶40 mg) in positive control group, respectively.All mice were killed after overdose anesthesia on the 17th day.Their eyeballs were made into samples and retinal tissue pathological sections with H-E dying method.The positive expressions of VEGF , COX-2, and MMP-2 were detected with immu-nohistochemical method .The fresh retinal tissue homogenate was prepared to detect the protein expressions of VEGF , COX-2, and MMP-2 in retinal tissue with western blot method ,and mRNA expressions of VEGF , COX-2, and MMP-2 were detected with real-time fluorescent quantitative polymerase chain reaction ( RT-PCR) .Results According to protein and mRNA expressions of VEGF , COX-2,and MMP-2 in retinal tissue among six groups , protein expressions of VEGF , COX-2, and MMP-2 in model group were significantly higher than those in blank group ( P <0.05 ) .Each protein expression in the high UA intervention group was significantly lower than that in the model group ( P <0.05 ) .Each protein expression in the high UA intervention group was not significantly different from that in the positive group ( P >0.05 ) .Each protein expression in the high UA intervention group was significantly lower than that in the low UA intervention group( P <0.05).Conclusions UA inhibited expressions of VEGF, COX-2, and MMP-2 in retinal ischemia model .UA also played an inhibitory role in the formation of neovascularization , and this role was positively correlated with UA dose .

AIM:To observe the expression of connective tissue growth factor(CTGF)in unilateral ureteral obstruction(UUO)rats,and to explore its pathogenic role in renal tubulointerstitial fibrosis.METHODS:48 Wistar rats were randomly divided into sham-operated and UUO group.The rats were sacrificed at day 1,3,7,and 14.The degree of tubulointerstitial damage was scored according to the Masson staining.The mRNA and protein levels of CTGF,transforming growth factor-?1(TGF-?1),collagen Ⅰ(Col Ⅰ),and plasminogen activator inhibitor-1(PAI-1)were detected by reverse transcriptional-polymerase chain reaction(RT-PCR)and immunohistochemistry,respectively.Expression of CTGF protein in the kidney was also assessed using Western blotting.RESULTS:TGF-?1 mRNA level began to increase as early as 1 day after UUO.This increase was followed by the elevation of CTGF mRNA level,which began to increase at third days after UUO(P

A potential pathological role of angiopoietins (Ang) in glomeruli following podocyte injury-induced progressive glomerulosclerosis was explored. Eighty male Wistar rats were randomly allocated into sham operation group (Sham, n = 25), Uninephrectomy group (UPHT, n = 25) and Uninephrectomy+Daunorubicin group (DRB, n = 30). In DRB group, daunorubicin (5 mg/kg) was injected via tail vein on the 7th and 14th day after uninephrectomy. At week 1, 2, 4, 6 and 8 respectively following establishment of the animal model, 5 rats in Sham group and UPHT group, and 6 in DRB group were taken respectively for determining 24-h urinary protein excretion rate (24hUPER), blood urea nitrogen (BUN) and serum creatinine (Scr). The sections of kidneys were examined by an electric microscope, PAS staining, immunohistochemical staining and in situ hybridization histochemistry. The results showed that 24hUPER, BUN and Scr in DRB group were more than those in Sham group and UPHT group at the same time points, and there was a trend towards an increase on level of GSI in DRB group from week 2 to week 8. Electric microscopy revealed that podocyte injury presented in DRB group. The expression of Ang1 mRNA and protein in glomeruli of DRB group was decreased, while the expression of Ang2 protein in glomeruli of DRB group increased. Meanwhile, the expression of Ang1 mRNA had a negative correlation with the expression of Ang2 mRNA, and the expression of Ang1 protein had a positive correlation with the expression of Ang1 mRNA, and had a negative correlation with 24hUPER, BUN, Scr, glomerular sclerotic index (GSI), the expression of Ang2 protein and CoIV protein. The expression of Ang2 protein had a positive correlation with the expression of Ang2 mRNA, and had a positive correlation with 24hUPER, BUN, Scr, GSI, the expression of CoIV protein. It was concluded that podocyte injury might lead to an alteration in the expression of Ang1 and Ang2 within glomeruli. Ang2 may get rid of inhibition from Ang1 for downregulation of the Ang1 expression, which facilitate upregulation of the Ang2 expression in glomeruli to promote progressive glomerulosclerosis in the rats.

To investigate the role and mechanisms of apoptosis and apoptosis signaling pathway in 5/6 nephrectomy rat model (SN(x)), the mRNA and protein levels of caspase-3, -8, -9 and apoptosis were detected by in situ end labeling (TUNEL), immunohistochemistry, RT-PCR, Western-blotting 1, 2, 4, 8, 12, 16, 26 and 40 weeks after 5/6 nephrectomy rat model was made respectively. The rats in the model group developed glomerular sclerosis and renal interstitial fibrosis. The number of the apoptototic cells in glomeruli, renal tubule and renal interstitium was remarkably higher in the model group than that in the control group (P < 0.05, P < 0.01). Changes of mRNA and protein level of caspase-3, -8, -9 had the same tendency and was up-regulated wavily in the rat model compared with the control group (P < 0.05). Peaks in model appeared on the 4th and the 40th week respectively. The growth amplitude of caspase-9 was remarkably higher than that of caspase-8. It is concluded that the development of 5/6 nephrectomy rat model was correlated with the apoptosis of glomeruli, renal tubule and renal interstitium. Both of death receptor and mitochondria signaling pathways are involved in the process and the latter might play a primary role.

Accumulating evidence suggests that the small G protein Rho and its downstream effector Rho kinase may play important roles in kidney biology. The present study examined the effects of a Rho-kinase inhibitor, fasudil, on daunorubicin-induced progressive glomerulosclerosis and explored the underlying mechanism by which fasudil ameliorates glomerulosclerosis. Thirty-six male SD rats were randomly allocated into sham-operation group (sham group, n=12), unilateral nephrectomy (UNX)+daunorubicin (DRB) group (model group, n=12), UNX+DRB+Fasudil group (treatment group, n=12). Two to four weeks after the establishment of the animal model, 6 rats in each group were taken randomly for the detection of 24-h urine protein excretion. Kidney sections were examined by HE and PAS staining, immunohistochemistry and transmission electric microscopy (TEM). The expression of Rho-kinase mRNA and P27 mRNA in kidney were detected by RT-PCR. It was found that the 24-h urine protein excretion in model group was increased significantly as compared with sham group (P<0.01). But this increase was significantly suppressed by fasudil (P<0.05). At 4 week, the foot process effacement in podocytes, mesangial proliferation and ECM accumulation were observed in model group, presenting as focal segmental glomerulosclerosis. But in the treatment group, the fasudil alleviated glomerular injury, with proliferating cell nuclear antigen (PCNA)-positive cell infiltration ameliorated and the expression of P27 increased. The expression of Rho-kinase mRNA was significantly enhanced in model group and was suppressed in treatment group. Moreover, fasudil up-regulated the mRNA expression of P27. Our study demonstrated that the glomerulosclerosis was substantially ameliorated by inhibiting the expression of Rho-kinase. It is suggested that Rho-kinase pathway is involved in the renal injury and the inhibition of Rho-kinase may constitute a therapeutic strategy for the treatment of renal injury.