Objective: To observe the effect of scraping therapy (ST) on the immune balance of serum helper T (Th) 1/Th2 cells in autologous nucleus pulposus transplantation non-compressive lumbar disc herniation (LDH) model rats, and explore the immune mechanism of ST in reducing LDH pain. Methods: Seventy-two male Sprague-Dawley (SD) rats were randomly divided into a model group, a sham operation group and a ST group, with 24 rats in each group. Autologous nucleus pulposus transplantation non-compressive LDH models were established in the model group and ST group, while the rats in the sham operation group underwent sham operation without model establishment. On the fifth day after the model was successfully prepared, rats in the ST group received ST, once every other day, 3 times as a course for a total of 3 courses. Six rats in each group were randomly selected to observe their pain thresholds, and peripheral blood of the rats was collected before the first scraping treatment and at the end of the first, second, and third courses of treatment. The serum was isolated and enzyme-linked immunosorbent assay (ELISA) was applied for the detection of rat serum interferon (IFN)-γ, interleukin (IL)-4 and IL-10. Results: Compared with the model group, the pain threshold in LDH rats in the ST group increased (P<0.05), the serum IFN-γ level was significantly reduced (P<0.05), but the levels of IL-4 and IL-10 did not change significantly (both P>0.05). At the end of the second and third courses of treatment, the IFN-γ/IL-4 ratio was negatively correlated with the pain threshold in the rats, and the IFN-γ/IL-4 ratio was significantly reduced in the ST group (P<0.01). Conclusion: ST can help suppress the Th1 immunity in LDH rats triggered by the autologous nucleus pulposus, restore the immune balance of Th1/Th2, and reduce the pain of LDH.

Objective To explore the inhibitory effect of rosiglitazone of peroxisome proliferator-activated receptor-?(PPAR?) agonist on aldosterone-induced mesangial cell(MC) proliferation.Methods Mouse primary MC were cultured and treated with aldosterone(100 nmol/L) in the presence or absence of rosiglitazone(1.0,2.5,5.0,10.0 ?mol/L).The incorporation of 3H-thymidine(3H-TdR) and cell count were used as the measure of MC proliferation.Cyclin D1 and cyclin A expression,PI3K and Akt phosphorylation were determined by Western blot analysis.Results 1.Aldosterone induced MC proliferation,as assessed by 3H-TdR incorporation and cell number,which were increased by 2.46-and 2.14-fold,respectively,in aldosterone-treated cells.Aldosterone-induced MC proliferation was inhibited by PPAR? agonist rosiglitazone in dose-dependent manner in mouse MC.2.Aldosterone induced cyclin D1 and cyclin A expression.Rosiglitazone reduced aldosterone-induced cyclin D1 and cyclin A expression in dose-dependent manner.3.Aldosterone induced PI3K/Akt activation in dose-dependent manner,incubation with 100 nmol/L aldosterone for 60 min,phosphorylation PI3K and Akt expression increased by above 3.0-fold.4.PI3K inhibitor LY294002 and Akt inhibitor significantly inhibited aldosterone-induced cyclin D1 and cyclin A expression.5.Rosiglitazone significantly inhibited aldosterone-induced PI3K/Akt activation,10 ?mol/L rosiglitazone almost completely blocked aldosterone-induced PI3K/Akt activation.Conclusion Rosiglitazone can block aldosterone-induced MC proliferation via inhibition of PI3K/Akt activation.

Objective To investigate the effect of c-Jun N-terminal kinase(JNK) specific inhibitor SP600125 on Angiotensin Ⅱ(AngⅡ)-induced transforming growth factor-?1(TGF-?1) and fibronectin (FN) expression in human mesangial cells (MC).Methods Human MC were isolated and cultured in vitro and were treated with AngⅡ in the presence or absence of JNK specific inhibitor SP600125.The protein was isolated or the supernate of medium was collected at the end of experiment.JNK,extracellular signal-regulated kinase(ERK1/2),and p38 mitogen-activated protein kinase(MAPK) activity were determined by Western blot method.TGF-?1 and FN were determined by enzyme linked immunosorbent assay(ELISA).Results SP600125 inhibited AngⅡ-induced Ser63 phosphorylation of c-Jun in a concentration-dependent manner,and JNK activity was reduced by 75% at 10 ?mol/L and by 90% at 20 ?mol/L.SP600125 had no effect on AngⅡ-induced ERK1/2 and p38 activity.TGF-?1 and FN protein were constitutively produced in MC,and production was significantly stimulated for 8 to 48 h after addition of AngⅡ.Preincubation of cells with SP600125(20 ?mol/L) significantly inhibited AngⅡ-induced TGF-?1 and FN production during this time period.SP600125 inhibited AngⅡ-induced production of TGF-?1 and FN in a concentration-dependent manner.Conclusion SP600125 inhibited AngⅡ-induced JNK activation and TGF-?1 and FN expression in human MC and may serve as the novel approach for the treatment of patients with chronic kidney disease.

AIM: To evaluate the effect of binocular visual function training in pediatric ocular trauma. METHODS: There were 76 patients (76 eyes) that were hospitalized with a primary diagnosis of ocular injury at the Affiliated Hospital of Medical College, Qingdao University between January 2006 and December 2009. Binocular visual function training was given after primary wound repair. Far stereopsis function were checked using AIT-1000 synoptophore fusion, and near stereopsis function was checked using Titmus stereogram.Binocular visual function was compared before and after training. RESULTS: Before binocular visual function training,26 eyes（34%）had no binocular vision, after training there were only 16 eyes（21%） without binocular vision. Before undertaking binocular visual function training with fusion, only 27 eyes (36%) had binocular vision, after the training there were 48 eyes (63%) with binocular vision. Before undertaking binocular visual function training with far stereopsis ,there were 23 eyes (30%) with binocular vision, after the training there were 29 eyes (38%). Before binocular visual function training with near stereopsis, there were 14 eyes (18%) with binocular vision, after the training there were 33 eyes (43%) with binocular vision. There was a significant difference in the number of patients with binocular vision before and after binocular visual function training. CONCLUSION:The training is useful for the reconstruction of binocular visual function in pediatric ocular trauma.

OBJECTIVETo study the proliferation and apoptosis of tetramethylpyrazine (TMP) on leukemic U937 cells and its possible mechanism.

METHODThe inhibitory effect of TMP on the proliferation of U937 cells was detected by CCK-8 assay. The cell apoptosis and cycle distribution were examined by the flow cytometry. The mRNA expressions of bcl-2 and P27 were determined by the Real-time PCR. Western blot was carried out to detect bcl-2, caspase-3, cyclin E1, CDK2 and P27 expressions.

RESULTTMP inhibited the proliferation of U937 cells in a dose-and-time dependent manner, with IC50 value of 160 mg x L(-1) at 48 h. In addition, TMP could induce the apoptosis of U937 cells and block the cell cycle in G0/G1 phase. According to the results of Real-time PCR and Western blot, TMP could down-regulate the expression of apoptosis-related molecule bcl-2, cycle-related protein cyclin E1 and CDK2 and up-regulate caspase-3 and P27.

CONCLUSIONTMP shows the effects in inhibiting the proliferation of leukemic U937 cells and inducing the apoptosis. Its mechanism may be related to the impacts on the cell cycle distribution, down-regulation of the bcl-2 expression, which finally activates caspase-3, starts the apoptosis path and causes the cell apoptosis.

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Cyclin-Dependent Kinase 2 ; analysis ; Humans ; Leukemia ; drug therapy ; Proto-Oncogene Proteins c-bcl-2 ; analysis ; Pyrazines ; pharmacology ; therapeutic use ; U937 Cells

Objective To compare the therapeutic effect of the combination of ~(99m)Tc-methnetium methylene diphosphunate and colloidal chromic,phosphate ~(32)p with the monotherapies in rats with adjuvant arthritis(AA).Methods In this study,50 Sprague-Dawley rats were randomly divided into five groups with 10 rats in each:normal control group(arthritis induced and treated with the same volume of normal saline via the same administration route),AA control group(arthritis induced with adjuvant and treated with normal sa- line),~(32)p colloid group(arthritis induced with adjuvant and treated with single intra-articular injection of col- luidal chromic phosphate ~(32)p 0.74 MBq and intra-peritoneal injection of normal saline every other clay),~(99m)Tc- MDP group(arthritis induced with adjuvant and treated with intra-peritoneal injection of ~(99m)Tc-MDP 2.5?10~(-3)?g/kg every other day and single intra-articular injection of normal saline),combination group(arthritis in- duced with adjuvant and treated with the combination of the two drugs).The diameter of the left hind ankle, serum levels of turnout necrosis factor(TNF)and interleukin-1?(IL-1?),and the pathological changes of an- kle joints were tested at different time points.Results The diameter of the left hind ankle at week 4 was smaller in the combination group than that of the ~(32)p colloid treatment alone group [(7.11?0.34)mm vs(7.57?0.29)mm,P

Objective To evaluate therapeutic effects and toxicity of advanced non-small cell lung cancer (NSCLC)treated by combining chemotherapy on ifosfamide(IFO)and vinorelbine(NVB).Methods 107 cases pa- tients with advanced NSCLC were enrolled.IFO was given in a dosage of 1.5g/m~2 on day 1 to 4.and NVB in a dosage of 25mg/m~2 on day 1 and 8.It was repeated every three or four weeks,up to two to four cycles.Results Two patients had complete response and 40 patients had partial response.The overall response rate was 47.7% ,the median survival time 10.3 months,1-year and 2-year survival rate was 42% and 12.3%,respectively.The main toxicity was bone marrow suppression.Conclusion The regimen is effective,sale and tolerable in advanced non- small cell lung cancer therapy.

No abstract available.
Angiotensin II* ; Angiotensins* ; Hydrocortisone* ; Insulin*

No abstract available.
Gastrins*

OBJECTIVETo evaluate the clinical efficiency of selective cyclo-oxygenase-2 (COX-2) inhibitor compared to traditional nonselective NSAIDs for the prevention of heterotopic ossification (HO) after total hip arthroplasty (THA).

METHODSBy searching Medline, Embase, CENTRAL (Cochrane Central Register of Controlled Trials) and Science Citation Index et al, only randomised controlled studies of selective COX-2 inhibitors VS nonselective COX-1 and COX-2 inhibitors for the prevention of HO after THA were included. The quality assessment of included studies was evaluated according to the standard of the Cochrane Collaboration, and the data were analysised by statistic software Stata 10.0. The HO incidence of both groups in different degrees was compared.

RESULTSFour eligible randomised controlled trials of totally 808 patients were included. Meta-analysis results showed that no statistically significant difference was found in overall incidence of HO (RR = 1.08, 95% CI: 0.71-1.64,P = 0.73), incidence of moderate severe HO (Brooker II and III) (RR = 0.83, 95% CI: 0.48-1.42, P = 0.49) and any grade of Brooker classification between two groups. In all included studies, 16 patients receiving nonselective COX inhibitor (4.4%) discontinued treatment because of gastrointestinal toxicity,whereas 10 patients in the selective COX-2 inhibitor group (2.7%) discontinued for gastrointestinal side effects.

CONCLUSIONThe selective COX-2 inhibitors are as equally effective as nonselective NSAIDs for the prevention of HO after THA. Considering the side effects of nonselective NSAIDs, selective COX-2 inhibitors were recommend for the prevention of HO after THA.

Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; therapeutic use ; Arthroplasty, Replacement, Hip ; adverse effects ; Cyclooxygenase 2 Inhibitors ; adverse effects ; therapeutic use ; Cyclooxygenase Inhibitors ; adverse effects ; therapeutic use ; Humans ; Ossification, Heterotopic ; prevention & control ; Randomized Controlled Trials as Topic