[Objective]The purpose of this study is to investigate articular cartilage injuries in patients undergoing arthroscopy of knee joint.[Method]From November 2004 to September 2005,568 patients underwent arthroscopy in the orthopedic department of Chinese PLA General Hospital.[Result]Totally 923 cases of articular cartilage injuries in 389 patients were documented,with the incidence rate of 68%.The main articular cartilage injuries were found on the medial femoral condyle(26%)and patella(25%).The incidence rate had signicant difference between patients over and under 40 years(88% VS 36.5%).Patients between 40 and 60 years were most susceptable to articular cartilage injuries.[Conclusion]Articular cartilage injuries are common in patients after arthroscopy.Early arthroscopy and treatment may benefit the patients.

Objective To evaluate the therapeutic effect of lentinan combined with conventional antituberculous therapy in women with pelvic tuberculosis.Methods A total of 90 women with pelvic tuberculosis were enrolled and recruited into a control group and a treatment group by random number table,45 in each group.The control group was treated with anti-tuberculosis program (2HRZE/4HRE),while the treatment group was treated with lentinan tablets on the basis of the control group.Both groups were treated for 6 months.Serum levels of carbohydrate antigen 125 (CA125) and erythrocyte sedimentation rates (ESRs) were determined before and after treatment,and the therapeutic effect was evaluated.Results After treatment,the serum CA125 level (28.61 ± 9.08 U/ml vs.39.72 ± 12.13 U/ml;t=4.919,P＜0.01) and the ESR (36.13 ± 8.33 mm/h vs.41.35 ± 12.45 mm/h;t=2.338,P＜0.05) in the treatment group were significantly lower than those in the control group.The negative rate of serum CA125 after treatment than before treatment in the treatment group (93.3％ vs.20.0％;X2=46.335,P＜0.01) and the control group (82.2％ vs.8.9％;X2=37.396,P＜0.01);but there was no difference in negative rate of serum CA125 after treatment between two groups (X2=1.6571,P=0.198).The total effective rate in the treatment group was significantly higher than that in the control group (93.3％ vs.77.8％;X2=4.406,P=0.036).Conclusion Lentinan combined with conventional antituberculous therapy is effective in treatment of pelvic tuberculosis in women.

Background Our previous study showed that the expression level of glial fibrillary acid protein (GFAP) increases in astrocytes and Müller cells of retina in chronic hypertensive eye,and this change was clarified to be associated with the damage process of the retinal ganglion cells (RGCs).Aquaporin 4 (AQP4) exists in neural glial cells,so we conjecture AQP4 plays a role in the regulating GFAP expression in glaucomatous eye.Objectives This study was to investigate whether AQP4 gene can regulate the expression of GFAP in retina and explore the effect of AQP4 on RGCs damage of glaucoma.Methods Chronic ocular hypertensive eye models were established by cauterizing the scleral venous in the left eyes of 30 male AQP4-/-mice and 30 male wild type (WT) mice with the same background,and the right eyes served as control eyes.The intraocular pressure (IOP) was measured with Icare rebound tonometer at 1 day,3,7,14 and 28 days respectively and the retinas were isolated from 6 of each types of mice at the corresponding time points.The expression of GFAP in the retina was detected by Western blot.The use and care of the experimental animals followed ARVO Statement.Results The IOP was significantly higher in the model eyes than that of the control eyes 1 day,3,7,14 and 28 days in both AQP-/-mice (t =15.29,16.02,13.77,14.34,12.40,all at P＜0.05) and WT mice (t =17.65,14.91,15.97,13.41,12.53,all at P ＜0.05).GFAP was expressed in the control eyes both of the AQP4-/-mice and the WT mice.The expressing level of GFAP (GFAP/β-actin) in retinas was 1.00±0.00,1.99±0.29,4.05±0.69,4.47±0.48,3.21±0.35 and 3.25±0.53 in the control eyes and 1-,3-,7-,14-,28-day model eyes of WT mice; and those in the AQP4-/-mice were 1.00±0.00,1.69±0.31,2.27 ±0.55,2.79 ± 0.39,1.93 ± 0.31 and 1.54 ± 0.40,with a significant difference in the expressing level of GFAP in various time points (F =9.54,P＜0.05).In addition,significant gradually elevation of GFAP expression were seen in the WT mice and gradually decline of GFAP expression was found in the AQP4-/-mice with the lapse of time (all at P＜0.05).No significant difference was seen in the expression of GFAP in the control eyes between the WT mice and AQP4-/-mice (P＞0.05).However,the expression level of GFAP in retina was significantly higher in the WT mice than that of A QP4-/-mice 3,7,14 and 28 days after operation (t =4.51,7.95,6.12,5.76,all at P＜0.01).tonelusions In chronic high IOP mice,AQP4 gene plays an important role in retinal damage by upregulating the expression of GFAP in retina and promoting the activation of RGCs.AQP4 probably is a new target of treatment of glaucoma.

Background Long-term administration of glucocorticoid drugs induces ocular hypertension in susceptible individuals probably.It has been verified that 1 1β-hydroxysteroid dehydrogenase type 1 (11β-HSD1),glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) can affect the generating of aqueous humor,but how they play the role in glucocorticoid-induced ocular hypertension is unclear.Objective This study was to investigate the relationship of expressions of 11β-HSD1 and steroids receptors in ciliary body and steroid-induced ocular hypertension.Methods Thirteen 12-16 week-old New Zealand albino rabbits were randomized to control group (5 rabbits) and experimental group (8 rabbits).Steroid-induced glaucoma models were induced by administration of subconjunctival injection of 5 mg dexamethasone solution(1 ml) and 0.5％ dexamethasone eye drops on alternate days in the left eyes for consecutive two months in the experimental group,and the equal volume of sterile normal saline solution was used in the same way in the control group.The successful criteria of model eyes was defined as rising of intraocular pressure (IOP) to ≥ 18 mmHg for over one week.Then,the animals were sacrificed by excessive anesthesia and the ciliary tissues were isolated for the assay of expressions of 1 1β-HSD1 protein by immunochemistry,and the expressions of 11β-HSD1 mRNA,GR mRNA and MR mRNA in ciliary body were semi-quantitatively detected by reverse transcription-PCR (RT-PCR).The experimental results were compared between the two groups.Results The IOP was normal in the first two weeks after administration of drugs,and no significant difference was found in IOP between the first week and the second week in the experimental group (q =0.469,P ＞0.05).From 3 through 5 weeks after injection,the IOP was gradually elevated,with the highest value of (18.87±0.77) mmHg in the fifth week.Significant differences were seen between the two groups at mentioned-above time points (q =10.535,20.353,28.681,all at P ＜ 0.01).11β-HSD1 protein was positively expressed in nonpigmented epithelial cells of ciliary tissue of rabbits in both groups,however,the expression intensity was weaker in the experimental group compared with the control group.The relative expressional values of MR mRNA,GR mRNA and 11β-HSD1 mRNA in the ciliary tissue were 2.22±0.78,0.64±0.11 and 0.47±0.16 in the experimental group,and those in the control group were 0.94±0.27,1.88±0.74 and 2.68±1.28,with significant differences between the two groups (t =6.070,P =0.004 ; t =5.170,P =0.007 ; t =5.540,P =0.005).Conclusions Corticosteroidinduced glaucoma probably is associated with the up-regulation of MR level and down-regulations of GR and 11β-HSD1 in ciliary body.

The over-expression of Polo-like kinase 1(Plk1)is critical in the producing and progressing of multi-ple human tumors and is recognized as an effective target for the development of novel anti-cancer drugs.Currently a variety of small molecules targeting ATP or substrates binding sites have entered different stages of clinical trials.Polo-box domain(PBD)is a unique domain of Plks which plays an important role in the sub-cellular location of Plks and also in the recognition of their substrates,therefore it has become an attractive target for the development of novel target-directed Plk1 inhibitors.In this paper,PBD function of Plk1 was intro-duced,the progress of small molecule and phosphoserine /phosphothreonine contained short peptide Plk1 inhibi-tors targeting PBD was summarized.Further development of this kind of inhibitors was also proposed.

Objective To investigate the expression of Toll-like receptor 4 (TLR4) of peripheral blood mononuclear cell (PBMC) in the different prognosis of patients with severe sepsis and its relation with endotoxin-tolerant.Methods Thirty-five patients with severe sepsis (severe sepsis group) and 15 healthy volunteers (control group),respectively stayed in ICU 24 h and physical examination in the day measured TLR4 expression of PBMC by flow cytometry and measured the serum of tumor necrosis factor (TNF)-α and interleukin (IL)-10 by enzyme-linked immunosorbentassay.Simultaneous separation of peripheral blood of PBMC,addition of 40 μ g/ml lipopolysaccharide (LPS) cultured for 24 h,and TLR4 expression of PBMC was measured in the same manner and the culture supernatant of TNF-α and IL-10.Results Thirty-five patients with severe sepsis survivor 25 cases (survivor group) and death 10 cases (death group),28 d death rate was 28.6％ (10/35).The TLR4 expression of PBMC in severe sepsis group was significantly lower than that in control group [(11.09 ± 8.90) MFI vs.(33.72 ± 12.59) MFI,P ＜ 0.01],the serum TNF-α and IL-10 in severe sepsis group were significantly higher than those in control group [(96.66 ± 45.33) ng/L vs.(2.53 ± 1.21) ng/L,(149.79 ± 67.15) ng/L vs.(34.56 ± 19.08) ng/L,P ＜ 0.01].There was no significant difference in TLR4 expression of PBMC between survivor group and death group (P ＞ 0.05).The TLR4 expression of PBMC in control group after LPS stimulation was significantly higher than that before LPS stimulation [(50.22 ± 19.23) MFI vs.(33.72 ± 12.59) MFI,P ＜ 0.05],survivor group and death group after LPS stimulation were significantly lower than those before LPS stimulation [(4.55 ± 2.30) MFI vs.(11.21 ±7.92) M FI and (5.46 ± 3.44) M FI vs.(10.15 ± 9.70) MFI,P ＜ 0.01].The culture supernatant of TNF-α,IL-10 in survivor group and death group were significantly lower than those in control group [(22.34 ± 8.27)and (19.49 ±5.35) ng/L vs.(88.70 ±34.21) ng/L,(54.29 ±32.89) and (98.04 ±40.26) ng/L vs.(146.56 ± 52.18) ng/L,P ＜ 0.01],but the culture supernatant of IL-10 in death group was significantly higher than that in survivor group (P ＜ 0.05).Conclusion Different prognosis of patients with severe sepsis have endotoxin tolerance and different inflammatory cytokine secretion abifity.

Aim To observe the effects of the ethyl ace-tate extract from Coreopsis tinctoria on glucose and lipid metabolism and liver, kidney function in diabetic rats. Method By high-sugar, high-fat diet combined with intraperitoneal injection of streptozotocin ( streptozoto-cin, STZ ) Type 2 diabetes SD rat model was estab-lished. Model rats were randomly divided into six groups ( control group, model group, three dose groups Coreopsis tinctoria extract:low, middle,high 0. 15 g· kg-1;0. 3 g·kg-1;0. 6 g·kg-1 , positive drug met-formin 0. 16 g · kg-1 group ) . The control group and the model group were given physiological saline and the remaining groups intragastric administration coreofosis tinctoria extrat. Random blood glucose and body weight of rats were measured weekly. After 4 weeks of admin-istration, The rats were killed and rat serum was col-lected to detect serum lipids ( TC/TG/HDL/LDL ) , liver and renal function indicators, serum insulin, and glycated hemoglobin levels. Result Coreopsis tincto-ria ethyl acetate extract effectively reduced the diabetic rats random blood glucose, glycated hemoglobin,serum triglycerides, LDL, total serum protein, serum creati-nine and uric acid levels, and increased serum white protein content in diabetic rats. Conclusion Coreop-sis tinctoria ethyl acetate extract can reduce blood glu-cose and lipid in diabetic SD rats and protect their liver and kidney function.

ObjectiveTo study the effect of α7 ( α7 AChR) agonist nicotine on regulating sensitivity of regular chemotherapeutic agent in cholangiocarcinoma cells,and explore the possible target.MethodsThe effect of nicotine and α-BTX pretreatment on the survival ability of cholangiocarcinoma cells was investigated when applied with 5-FU by using MTT and Flat cloning formation experiment.ResultsApplied with 5-FU,in various con centrations nicotine stimulating group( 10-3 g/L,10-4 g/L,10-5 g/L ),the survive rate of QBC939 was 128％,124％,118％,while that in α-BTX stimulating group and combined stimulation group was 92％,94％,93％,92％,respectively.The cloning formation ability of nicotine- stimulating group (6.2 ± 0.40) was significantly higher than α- BTX stimulating group (3.2 ± 0.20 ),combined stimulation group ( 3.2 ± 0.20 ) and control group ( 3.4 ±0.33).ConclusionNicotine can prevent chemotherapy-induced apoptosis,and improve cholangiocarcinoma cell survival via α7 nicotine acetylcholine receptor in vitro.

Objective To investigate the role of p53 in the regulation of heat shock protein(Hsp)84 and 86,and the correlation of their functional imbalances with accelerated brain aging and with suppressed tumorigenesis in SAMP8 mice(senescence accelerated mouse prone 8).Methods The mRNA and protein expressions of Hsp84 and Hsp86,and protein expressions of p53 pathway-related proteins(p21 and MDM2)in hippocampus of SAMP8 mice and their control SAMR1(senescence accelerated mouse resistant 1)mice were determined.Murine Neuro-2a cells were treated with 20 μmol/L Aβ25-35,and then mRNA expressions of p53,Hsp84 and Hsp86 in these cells were detected.Neuro-2a cells were co-transfected with p53 siRNA and pHsp84-Luc or pHsp86-Luc plasmid and treated with 20 μmol/L Aβ25-35,then promoter activity of Hsp84 and Hsp86 were detected in these cells.After co-transfection with pcDNA3.1-p53 or pcDNA3.1-p53DD and pHsp84-Luc or pHsp86-Luc plasmids,the neuro-2a cells were treated with 20 μmol/L Aβ25-35.Then promoter activity of Hsp84 and Hsp86 were detected in these cells at different concentrations of p53.Results The mRNA levels of Hsp84 and Hsp86 in the hippocampus of SAMP8 mice were significantly declined,which were 13.51% and 16.13% of SAMR1 mice,respectively(all P<0.01).Compared with the SAMR1 mice,the protein expressions of Hsp84 and Hsp86 in the hippocampus of SAMP8 mice were obviously declined(all P<0.01).Whereas,p53 pathway-related protein p21 expression was increased and MDM2 expression was decreased(all P<0.01).The mRNA expression of p53 in AD cells was significantly increased by 58%(P<0.01),whereas Hsp84 and Hsp86 mRNA levels were significantly decreased by 32% and 41%,respectively as compared with the normal cells(all P<0.05).Inhibition of p53 in AD cells could increase promoter activity of Hsp84 and Hsp86 significantly in a concentration-dependent manner(both P<0.05),whereas overexpression of p53 in the cells could lead to decreased promoter activity of them in a concentration-dependent manner(both P<0.05).Conclusions The p53 can negatively regulate the expressions of Hsp84 and Hsp86.The activity of p53/p21 pathway is increased,while Hsp84 and Hsp86 are inhibited in the brain of SAMP8 mice.Functional imbalance between p53 and Hsp84/86 might be the part of reasons causing accelerated aging and suppressed tumorigenesis in SAMP8 mice.

Objective: To observe the effect of Tongxinluo (TXL) on homocysteine-induced rat’s cardiac micro vascular endothelial cell (RCMECs) injury and to study the oxidative stress mechanism. Methods: Primary RCMECs were cultured with tissue explants process, cell morphology was observed by inverted microscope and the cell was identiifed by CD31 immunolfuorescence method. RCMEC injury model was established by Homocysteine (Hcy) induction and the cells were divided into 5 groups: Control group, with normal cells, Hcy group, the cells were treated by Hcy at 10 mmol/L, Low-dose TXL group, Hcy treated cells were cultured with TXL at 100 mg/L, Middle-dose TXL (200 mg/L) group and high-dose TXL (400 mg/L) group. Cell survival rates were detected, supernatant levels of superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were examined, intracellular protein expressions of reactive oxygen species (ROS) and endothelial nitric oxide synthase (eNOS) were detected and mRNA expression of endothelin-1 (ET-1) was measured in different groups respectively. Results: Compared with Control group, Hcy group showed decreased cell survival rate (74.61 ± 2.88)% vs (100.00 ± 2.07)%, increased supernatant level of MDA (4.10 ± 0.18) nmol/ml vs (1.92 ± 0.10) nmol/ml, reduced SOD activity (7.55 ± 0.71) U/ml vs (20.77 ± 0.68) U/ml, elevated ROS level(38.17 ± 10.28) % vs (19.83 ± 2.97) %, up-regulated mRNA expression of ET-1 and down-regulated protein expression of eNOS. Compared with Hcy group, the above indexes were improved in each TXL group at different levels. Conclusion: TXL could decrease Hcy induced RCMECs injury, such protection was conducted by reducing the oxidative stress mechanism in cells.