Objective To observe the change of Wnt-β-catenin signaling's location and expression in kidney repair after acute kidney injury induced by ischemla reperfusion (I/R).Methods Ischemia reperfusion injury in BAT-gal reportor mice was made and blood sample was taken from tails on the 1th day after injury. Mice were sacrified on the 2th or 7th day and kidneys and blood were collected. Renal pathological change was observed by PAS stain. The changes of location and expression of Wnt-β-catenin signaling were detected by immunofluorescence costainning X-gal-LTL, X-gal-NKCC2, X-gal-DBA respectively. The protein expressions of the Wnt4 and co-receptor Lrp6 were assessed by Western blotting. Results PAS-stained kidney sections showed desquamative or flattened epithelia, necrotic debris on day 2 and regenerating tubules on day 7. An injury-induced enhancement of the Wnt pathway response (X-gal staining) in kidney cortex and out-medulla. Immunolabelling of kidney sections from injured BAT-gal mice revealed that X-gal staining was detected in kidney epithelial cells (double-labelled with LTL or NKCC2). Western blotting showed the Wnt4 protein was up-regulated and phospho-Lrp6, indicative of active canonical Wnt signaling, was noted in kidney cortex from day 2 after I/R, but in control kidney cortex pLrp6 was not detected. Conclusion Wnt-β-catenin signaling is activited after acute kidney I/R injury and is required for tubular epithelial repair and regeneration following kidney I/R injury.

Organophosphate pesticides(OPs)are used extensively in agriculture,it became the most heavily used insecticides in China after the use of organochlorine pesticide was restricted in 1980s in China.Recent years,with an increasing usage of organophosphate pesticides in China,much concern has been showed for the level of OPs in human body and the adverse effects of OPs on human health especially on fetuses and children have raised a great.The level of OPs in children and the adverse effects of OPs exposure on neurobehavioral development of children were reviewed in the present article.

Objective To investigate the clinical efficacy of joint-corresponding point selection plus exercise acupuncture in treating acute ankle sprain.Method Enrolled 70 patients with acute ankle sprain were randomly allocated to two groups.The treatment group received joint-corresponding point selection plus exercise acupuncture and the control group,elastic bandage fixation.Both groups were given ice compress,mobilizationand elevation as auxiliary measures.Treatment was provided seven days as one coursefor a total of two courses.The pain, tenderness, swelling andrange of activitieswere scored in the two groups of patients before and after treatment.Thetherapeutic effects were compared.Result The total efficacy rate was 88.6% in the treatment groupand54.3% in the control group.The therapeutic effect was significantly better in the treatment group than in the control group (P<0.01). Joint pain, tenderness, swelling and activity scores decreased in the two groups after treatment (P<0.01). Joint tenderness and activity scores were lower in the treatment group than in the control group after treatment (P<0.01).Conclusion Joint-corresponding point selection plus exercise acupuncture has clinically a marked therapeutic effect on acute ankle sprain.

Objective To investigate the signal mechanism of protein kinase C alpha(PKC-α)participated in enhanced expression of type Ⅰ inositol 1,4,5-trisphophate receptors (IP3 RI) induced by tumor necrosis factor alpha(TNFα),in order to delineate the mechanisms of decreased glomerular filtration rate (GFR) in hepatorenal syndrome caused by TNFα.Methods The glomerular mesangial cells (GMCs)line from rats was chosen as experimental material.GMCs were divided into control (D),TNFα-2 h,TNFα-4 h,TNFα-8 h,and TNFα-24 h groups.Moreover,another two groups were sanflngol-8h (S),TNFα + Sanfingol-8h(TS)groups.The effect of TNFα on the expression of IP3RI was detected by immunocytochemical staining,Western blotting,teal time-polymerase chain reaction (PCR) assays.Results Immunocytochemical staining demonstrated that IP3 RI was mainly distributed in cytoplasm of GMCs.Enhanced positive staining was determined in all TNFα-treated groups,especially in TNFα-8 h group.Western blotting demonstrated that the expression of IP3RI protein was significantly higher in TNFα-4 h,TNFα-8h and TNFα-24 h groups than control group(4 h:1.82 ± 0.63 ; 8 h:2.95 ± 0.66 ; 24 h:2.48 ± 0.72 ; D:1 ±0.02 ; F =9.24,P ＜ 0.05).The expression of IP3 RI protein was the highest in TNFα-8 h and TNFα-24 h groups(P ＜0.05).No difference was found among S,TS,and control groups(S:1.39 ±0.65; TS:1.35± 0.37 ; P ＞ 0.05).Real time-PCR found the expression of IP3 RImRNA was significantly higher in all TNFα-treated groups than control group(2 h:3.35 ± 1.97; 4 h:3.16 ± 1.35; 8 h:3.70 ± 1.76; 24 h:4.49±1.70; D:1 ±0.01; F =6.167,P ＜0.05).No difference was found among all TNFα-treated groups(P ＞0.05).No difference was found among S,TS,and control groups(S:1.53 ±0.79; TS:1.32 ± 0.38 ; P ＞ 0.05).Conclusions IP3 RI was mainly distributed in cytoplasm of GMCs.TNFa could enhance the expression of IP3 RI protein and IP3 RI mRNA,which could be blocked by sanfingol,a PKCα inhibitor.It might be an important signal in the mechanisms of GFR decrease caused by TNFα in hepatorenal syndrome.

Objective To investigate the effect of tumor necrosis factor-α (TNF-α) on intracellular calcium concentration ([Ca2 +] i) and the contraction of glomerular mesangial cells (GMCs),and prove that hypercontractility of GMCs induced by TNF-α in hepatorenal syndrome(HRS) was connected with inositol 1,4,5-trisphophate receptors (IP3Rs).Methods GMCs were divided into TNF-α-treated 0 h,4h,and 24 h groups.Another 3 groups were blocked by 2-APB.The effect of TNF-α on [Ca2 +] i was identified and observed whether it could be blocked by 2-APB.Contraction of GMCs was determined by accessing the surface area of cells before and after contraction.Results TNF-α significantly increased ET-induced calcium release,in that we found higher [Ca2 +] i after stimulated by ET in TNF-α-treated 4 h group and 24 h group[4 h:(648.08 ±267.11) nmol/L; 24 h:(879.30 ±-260.29) nmol/L; 0 h:(619.93 ±258.94)nmol/L,F =5.486,4 h vs 0 h:P ＜ 0.05 ; 24 h vs 0 h:P ＜ 0.05 ;24 h vs 4 h:P ＞ 0.05].This phenomenon can be totally blocked by 2-APB in all groups.The change in planar surface area in response to ET was slightly in control cells but significantly enhanced in TNF-α-treated cells [4 h:(2198 ± 340)μm2; 24h:(2260±553)μm2; 0 h:(2436±474)μm2,F =4.001,4 h vs0 h:P ＜0.05; 24 h vs0 h:P ＜0.05;24 h vs 4 h:P ＞ 0.05].Conclusion TNF-α can enhance ET-induced sarcoplasmic reticulum Ca2 + release and increase the contractile responses of GMCs to ET,which is associated with IP3Rs.TNF-α is responsible for hyperconstractility of glomeruli in HRS.

Nucleoside analogues have been the mainstay of clinical treatment of herpes simplex virus 1 (HSV-1) infections since their development. However, the emergence of drug resistant strains has underlined the urgency of the discovery of novel anti-HSV-1 drugs. Natural products, which provided many novel drug leads, are known to be an important source of anti-HSV-1 agents. Herein, we present an overview of natural products with anti-HSV-1 activities isolated from a variety of plants reported in recent years. Several different compounds, mainly belonging to the three groups of polysaccharides, polyphenols and terpenes, showed antiviral effects against HSV-1, indicating their potential to be promising anti-HSV-1 agents.

Objective:To investigate the effect of TGF-? on the expression of type Ⅰ inositol 1,4,5-triphosphate receptor in WB rat liver epithelial cells.Methods:The expression of type Ⅰ inositol 1,4,5-triphosphate receptor protein and mRNA were detected by Western blot and RT-PCR in WB rat liver epithelial cells in vitro stimulating with TGF-?.Results:The expression level of type Ⅰ inositol 1,4,5-triphosphate receptor protein and mRNA in WB rat liver epithelial cells were both increased after stimulating with TGF-? in several time points and reached the highest at 8 h stimulated, and then decreased.Conclusion:TGF-? enhance the IP_3R1 protein and mRNA expression in WB rat liver epithelial cells.

AIM: Currently available anti-scarring regimens for glaucoma filtration surgery have potentially blinding complications and safer alternatives would be beneficial. This experiment is to investigate the effect of TGF-β2 antisense oligodeoxynucleotide on differentiation, proliferation of subconjunctival fibroblast following glaucoma filtration surgery.METHODS: Glaucoma filtration surgery were performed on both eyes of 28 rabbits. TGF-β2 antisense oligodeoxynudeotide was subconjunctivally injected in the right eyes (A group), and TGF-β2 missense oligodeoxynucleotide (B group)or PBS(C group) was used at the same method in the left eyes as controls. Rabbits were killed at 4,7,14 and 28 days after surgery. Intraocular pressure (IOP), bleb characteristics were recorded at different time point. Subconjunctival fibroblasts were examined by immunohistochemistry and electron microscopy.RESULTS: The IOP of rabbits in group A was significantly lower at 14 days (6.74± 1.18 mmHg) and 21 days (8.15± 1.97mmHg) after operation than the IOP in group B (8.53± 1.04,9.72± 1.09 mmHg)(P ＜0.01) and group C(8.79± 1.21, 9.43±1.27 mmHg) (P ＜0.05). The mean bleb survival time was longer (17.2 days) in group A than that of group B (14.5 days) and group C (13.5 days)(P＜0.05). The population of the cells expressing α -smooth muscle actin(α -SMA) and proliferating cell nuclear antigen (PCNA) was significantly reduced in group A compared with the group B and C. The ultrastructure of fibroblast was not altered by TGF-β2 anti-sense oligodeoxynucleotide.CONCLUSION:TGF-β2 antisense oligodeoxynucleotide can prevent the scar formation after glaucoma surgery by inhibit the differentiation and proliferation of subconjunctival fibroblast. It could be a potentially useful anti-scarring alternative for the prevention of late surgical failure.

Dengue (DEN) virus is a member of the family flaviviridae which consists of a group of enveloped viruses with a single-stranded positive-sense RNA genome. DEN virus infection is initiated by the binding of envelope protein E to cellular receptor,followed by replication in cytoplasm which associated with a range of induced membrane structures. Further characterization of the DEN replication complex (RC) showed the involvement of NS1, NS2A, NS3, NS4A, and NS5 proteins as the viral replicase. The DEN virion maturation is associated with the cleavage of precursor of protein C by NS2B/NS3 protease and the glucosylase-mediated N-linked oligosaccharide trimming of prM, E protein. This review summarizes recent advance in research on DEN virus life cycle, emphasizing cellular receptor, RNA replication and virion assembly.

Objective To discuss digital subtraction angiography(DSA)findings and interventional treatment of broncho-costoarterial pulmonary circulation fistula(BPF).Methods Fifty one patients with massive hemoptysis were undergone DSA showing 19 cases with BPF.All BPF were cmbolized with 500～700?PVA, silk particles and segments,and steel coil;separately or in combination according to shunt orifice size and blood flow velocity.Results There were 4 types of BPF demonstrated by DSA according to feeding and drainage vessels,including 13 cases of bronchial artery-pulmonary artery shunt(AAS),2 cases of bronchial artery-pulmonary venous shunt(AVS),3 cases of intercostal artery-pulmonary artery shunt(IAPS)and 1 case of bronchial arteriovenous malformatoin(B-AVM).All patients were followed up for 1～4 years,with 18 cases of complete symptomless during 7 days postoperatively obtaining,the effective rate of 94.7%.There were 3 recurrent cases within 1 year with the recurrent rate of 15.79%.Conlusions BPF is the main factor for inducing and aggrevating pulmonary hemoptysis and interventional embolization serves as a safe and effective treatment.The method could be used repeatedly for recurrent cases and furthermore emphasis should be put on treating the primary pulmonary diseases simultaneously.(J Intervent Radiol,2007,16:84-87)