OBJECTIVE：To study the therapeutic effect and safety of domestic tolterodine tartrate in treating patients with urinary bladder overactivity.METHODS：56 cases of bladder overactivity were divided into two groups randomly：tolterodine and control(oxybutynin)group.The course of treatment was 6 weeks.RESULTS：The effect of tolterodine in treatment group was comparable to that of oxybutynin in control group,however,the adverse reactions in oxybutynin group were more common than those in tolterodine group.CONCLUSION：Tolterodine is a suitable drug to treat bladder overactivity.

AIM:To assess the protective role of melatonin(MEL)in a rat model of oleic-induced acute lung injury.METHODS:Twenty-four rats were randomly allocated to three groups as follows:saline(NS)injection group,oleic acid(OA)injection group and MEL plus OA injection group,the lavage protein,lung wet-to-dry weight ratio,malondialdehyde(MDA)content,superoxide dismutase(SOD)activity and lung histopathology were examined.RESULTS:(1)Injection 0.15 mL/kg of OA led to a severe acute lung injury(ALI),characterized by significantly increasing in lavage protein,lung coefficient(P＜0.01),and by histopathological alterations which presented hemorrhage,edema.thickened alveolar septum and the existence of inflammatory cells in alveolar spaces;(2)Infusion of MEL(20 mg/kg,intraperitoneally for 60 min before the oleic acid)markedly alleviated above-mentioned symptom induced by OA,consistent with decrease of MDA level(P＜0.01) and the increase of SOD activty(P＜0.01).CONCLUSION:Pre-treatment with MEL can attenuate the OA -induced ALI in rats via cleaning and preventing the formation of free radicals and further lessening the increase of alveolocapillary membrane permeability,these data suggest that MEL may be effective in the prevention of ALI.

Objective To evaluate the in vitro activity of seven imidazole antifungals against clinical isolates of common Candida species.Methods According to the Clinical and Laboratory Standards Institute (CLSI) microdilution method M27-A3,the in vitro activity of luliconazole,ketoconazole,miconazole,econazole,clotrimazole,sertaconazole and bifonazole was determined among 183 clinical isolates belonging to 5 species of Candida.Results The minimal inhibitory concentration range was 0.03-8 (geometric mean:0.067) mg/L for ketoconazole,0.03-16 (geometric mean:0.071 ) mg/L for miconazole,0.03-8 (geometric mean:0.207) mg/L for econazole,0.03-8 (geometric mean:0.061 ) mg/L for clotrimazole,0.03-16 (geometric mean:0.187) mg/L for sertaconazole and 0.03 -＞16 (geometric mean:1.050) mg/L for bifonazole. Luliconazole exhibited a superior activity against the 5 species of Candida in vitro,with the MIC range being 0.03-8 mg/L,geometric mean MIC 0.087 mg/L,MIC50 0.06 mg/L and MIC90 0.5 mg/L,respectively.However,some Candida isolates were identified to be relatively insensitive to these tested antifungals,including luliconazole.Conclusion All the tested imidazole antifungals,except for bifonazole,show an excellent activity against Candida species in vitro,but there exist a few Candida strains with relative insensitivity.

Objective To investigate whether human neutrophils kill Candida albicans through recognition of insoluble β-glucan in cell walls of C.albicans (CalG) by dectin-1,a C-type lectin receptor.Methods Neutrophils were obtained from peripheral blood of healthy human subjects and cultured in vitro.Real-time PCR was carried out to quantify the mRNA expressions of dectin-1 and Toll-like receptor 2 (TLR2) in neutrophils challenged with CaIG of 100 mg/L for 1,6,and 24 hours.A Fluoro hydrogen peroxide (H2O2) detection kit was used to determine H2O2 levels in some neutrophils exposed to CaIG (100 mg/L) for 15 minutes,2 hours,6 hours,as well as in some neutrophils preincubated with laminarin (a dectin-1 inhibitor) of 100 mg/L and 50 mg/L for 30 minutes followed by challenge with CaIG of 100 mg/L for 2 hours.Colony forming units (CFUs) were counted after the incubation of C.albicans with neutrophils pretreated with laminarin of 100 mg/L and 50 mg/L for 30 minutes.Results The relative mRNA expression level of dectin-1 was 2.8195 + 0.1669,5.4859 + 0.7244 and 3.6041 + 0.5372 in neutrophils challenged with CaIG for 1,6 and 24 hours,respectively,significantly higher than that in unchallenged neutrophils at these corresponding time points (all P ＜ 0.01).The level of H2O2 was (64.55 + 15.67),(290.34 + 30.56),and (208.54 ± 26.88) μ mol/L respectively in neutrophils treated with CaIG for 15 minutes,2 hours,and 6 hours respectively,compared to (22.05 ± 3.99) μmol/L in untreated neutrophils (all P ＜ 0.01).The pretreatment with laminarin of 100 and 50 mg/L attenuated the release of H2O2 in CaIG-treated neutrophils by 73％ ((80.45 + 22.41) μ mol/L,P＜ 0.01) and 45％ ((130.42 + 44.55) μmol/L,P＜ 0.01),respectively,compared with neutrophils treated with CaIG only.The fungicidal activity of neutrophils against C.albicans was also significantly inhibited by pretreatment with laminarin of 50 and 100 mg/L (both P＜ 0.01).Conclusions Dectin-1 may be involved in the secretion of H2O2 as well as killing of C.albicans by human neutrophils,which may provide a preliminary evidence for adoptive transfer of neutrophils as an approach to the treatment of systemic C.albicans infection.

Objective To study the damage to striatum in patients perorally addicted to compound codeine phosphate solution by using the brain dopamine transporter SPECT imaging. Methods Patients p erorally addicted to compound codeine phosphate solution ( n = 29 ) and addicted to heroin ( n = 27 ), as well as healthy volunteers (n = 31 ) were included in the study. Each of them underwent dopamine transporter (DAT) SPECT imaging with 99Tcm-2β-[N, N'-bis-( 2- mercaptoethyl ) ethylenediamino] methyl, 3β-(4-chlorophenyl)tropane (99Tcm-TRODAT-1). The striatum volume (V, cm3), mass (m, g) and radiactivity ratio (Ra) of striatum to whole brain were calculated using physio-mathematical modeling method.R esults Bilateral striatum of healthy volunteers showed typical "panda eyes" pattern and the distribution of DAT was uniform and symmetrical. Bilateral striatum of patients addicted to compound codeine phosphate showed impaired tracer uptake, similar to those addicted to heroin. The V, m and Ra of bilateral striatum of patients addicted to compound codeine phosphate were (23.68 ±4.94) cm3, (24.87 ±5.19) g and (5.01 ±0. 88 ) %, respectively, which were significantly lower than those of healthy controls: ( 35.39 ± 4.42 ) cm3,(37.16 ±4.64) g and (7.93 ±0.86)% (t = -9.69, -9.69, - 13.01, all P =0.000), but significantly higher than those addicted to heroin: ( 18.87 ± 4.66 ) cm3, ( 19.81 ± 4.90 ) g and (4.26 ± 1.02 ) % ( t =3.74, 3.74, 2.96, P = 0.000, 0.000, 0.005 ). Conclusion Long-term peroral intake of compound codeine phosphate solution may damage the function of cerebral striatum, which is someway similar to though less severe than, the impairment caused by heroin.

Background A main cause of visual impairment in proliferative diabetic retinopathy (PDR) is vitreous hemorrhage and retinal detachment due to contraction of fibrovascular membrane.To explore the pathogenic mechanism of fibrovascular membrane is a new target for the prevention and management of PDR.Objective This study was to determine the change in expression of vascular endothelial growth factor (VEGF),connective tissue growth factor(CTGF) and pigment epithelium derived factor(PEDF) in the proliferative membranes of patients with PDR after intravitreal injection of avastin,an anti-VEGF agent.Methods This study was approved by the Medical Ethic Committee of Tianjin Medical College,and written informed consent was obtained from each patient before enrollment.A prospective randomized-controlled study was designed.Twenty-six eyes of 24 patients with PDR scheduled for surgery were enrolled from January to June,2008 in Tianjin Medical College Eye Hospital.The patients were randomized into the simple vitrectomy group and avastin injection combined with vitrectomy group,with matched gender,age and disease duration.1.25 mg (0.05 ml) of avastin was intravitreally injected prior to surgery,and vitrectomy was performed 10 days after injection in the avastin injection combined with vitrectomy group,and only vitrectomy was given in the simple vitrectomy group.Preretinal membrane was collected during the surgery.Expression of VEGF,CTGF and PEDF in the preretinal membranes was assayed by immunochemistry.Results VEGF,CTGF and PEDF were expressed in the cytoplasm.The rate of VEGF expression in the preretinal membranes was 30.77％ in the avastin injection combined with vitrectomy group,showing a significant reduction in comparison with the simple vitrectomy group(100.00％)(U =4.000,P＜0.01).The rate of expression CTGF was remarkable elevated in the avastin injection combined with vitrectomy group compared with the simple vitrectomy group (92.31％ vs.62.54％)(U=7.500,P=0.048).However,no significant difference was found in the expression rate of PEDF between the two groups(100.00％ vs.92.31％) (U =65.500,P =0.299).Conclusions The results suggest that intravitreal injection of anti-VEGF drugs resulted in the decrease of VEGF expression and increased CTGF expression in proliferative membranes from patients with PDR.

Objective To evaluate the using of either 225 or 150 microgrammes of mifepristone combined with misoprostol for termination of second-trimester gestation(16～24 weeks).Methods 180 women requesting voluntary induced abortion during gestation 16～24 weeks were randomised to three groups,group 1:oral mifepris- tone 225rag,group 2:oral mifepristone 150mg,and group 3:injected 100rag rivanot by amniocentestis.The total suc- cess rate,once success rate,the interval of having-medicine to uterine-constraction,the volume of bleeding within 2 hours after labour and cervical laceration rate were observed.Results The once success rate of induced labour in group 1 was higher than that in group 2 and group 3(P

Objective To investigate the effects of Candida albicans on the expression of tumor necrosis factor-α(TNF-α)and activation of the intracellular signaling molecule p38 mitogen-activated protein kinase(p38MAPK)in a human acute monocytic leukemia cell line THP-1. Methods Some THP-1 cells were divided into several groups in vitro: two C. albicans groups treated with 105 CFU/ml and 106 CFU/ml heat-killed C. albicans respectively, a lipopolysaccharide (LPS)group treated with 100 μg/L LPS, a blank control group treated with RPMI 1640 medium, two dexamethasone-inhibited groups pretreated with 40 μg/L dexamethasone for 30 minutes followed by treatment with 106 CFU/ml heat-killed C. albicans and LPS respectively. After treatment for 1, 3 and 6 hours, real-time fluorescence-based quantitative PCR was performed to measure TNF-α mRNA expression in THP-1 cells in the above groups. Enzyme-linked immunosorbent assay(ELISA)was conducted to determine the level of TNF-α protein in the supernatant of THP-1 cells treated with 106 CFU/ml heat-killed C. albicans, 100 μg/L LPS or RPMI 1640 medium(blank control group)for 24 hours. Western blot was performed to measure the protein expression of p38MAPK and phosphorylated p38MAPK in THP-1 cells after treatment with 106 CFU/ml heat-killed C. albicans or RPMI 1640 medium (blank control group)for 30 and 60 minutes. Statistical analysis was carried out by using two-way analysis of variance, one-way analysis of variance and the least significant difference(LSD)-t test. Results Significant differences were observed in the mRNA expression level of TNF-α among the C. albicans groups, LPS group and blank control group (F = 110.98, P < 0.001). The mRNA expression level of TNF-α in THP-1 cells increased over time in a time-dependent manner after C. albicans treatment, with significant differences among different time points (F = 701.680, P < 0.001). Compared with the blank control group, both 106-CFU/ml C. albicans group and LPS group showed a significant increase in TNF-α protein expression (6385.70 ± 533.99 ng/L and 3212.06 ± 353.00 ng/L vs. 147.10 ± 0.53 ng/L, P < 0.001 and 0.005, respectively). An obvious increase was observed in the expression level of phosphorylated p38MAPK protein, but no significant changes were noted in that of p38MAPK protein, in THP-1 cells treated with 106 CFU/ml C. albicans for 30 and 60 minutes compared with the blank control group. The mRNA expression level of TNF-α significantly decreased in dexamethasone-pretreated 106-CFU/ml C. albicans group and LPS group compared with those without dexamethasone pretreatment(3.77 ± 0.62 vs. 208.50 ± 10.50, 6.20 ± 1.93 vs. 161.35 ± 1.65, both P < 0.001). Conclusions Heat-killed C. albicans can induce the activation of p38MAPK in and secretion of TNF-α by human THP-1 cells, which then participate in the innate immune response against C. albicans.

Objective To identify the helper plasmids from HEP-Flury strain rabies virus that could encapsidate the full-length genome of CTN strain. Methods Four overlapped fragments covering the full-length genome of rabies virus CTN strain were cloned into expression vector. A recombinant full-length genome plasmid (pCTN-GFP) contained the full-length genome of the CTN strain expect for ψ gene which was replaced by GFP gene was then constructed using restriction enzyme cleavage and ligation in vitro. In order to obtain the recombinant rabies virus CTN-GFP, the pCTN-GFP was transfected with helper plasmids carrying N, P, L gene of HEP-Flury strain. Results The four gene fragments of the genome were amplified and cloned into the expression vector. The recombinant genome cDNA plasmid pCTN-GFP was constructed and subjected to restriction endonuclease digestions. After sequenced to assure no absence and mutations compared with their parental viruses, it was ready for virus rescue. After the transfection of both pCTN-GFP and the helper plasmids from HEP-Flury strain into BHK-21 cells, the recombinant rabies virus CTN-GFP was rescued and confirmed by fluorescence analysis and RT-PCR, which demonstrated that the CTN-GFP was recovered from cloned cDNA. Conclusion The proteins of HEP-Flury strain rabies virus could encapsidate and transcribe the CTN strain rabies virus RNA genome.

Objective: To observe the effect of electroacupuncture (EA) pretreatment on the protein expression of c-fos in fastigial nucleus (FN) and lateral hypothalamus area (LHA) in rats with acute myocardial ischemia-reperfusion injury (MIRI), and to explore the role and mechanism of FN and LHA in EA at the Heart Meridian fighting against acute MIRI reaction. Methods: Seventy Sprague-Dawley rats were randomly divided into a sham operation group, a model group, an EA-Heart Meridian group and an EA-Lung Meridian group, with 14 rats in each group; an LHA lesion plus EA-Heart Meridian group (LHA+EA-Heart Meridian group) and a FN lesion plus EA-Heart Meridian group (FN+EA-Heart Meridian group), with 7 rats in each group. Except the sham operation group, the left anterior descending branch of coronary artery was ligated to establish acute MIRI rat models in the other 5 groups. In the three groups with EA-Heart Meridian treatment, Shenmen (HT 7) and Tongli (HT 5) were selected; Taiyuan (LU 9) and Lieque (LU 7) were selected in the EA-Lung Meridian group. All the EA groups received EA stimulation prior to modeling, with 1 mA in current intensity and 2 Hz in frequency, 20 min each time, once a day for a total of 7 d. The sham operation group and the model group did not receive EA stimulation. The electrocardiogram was observed in the rats to analyze the ST-segment deviation and cardiac arrhythmia score. The expression of c-fos protein in FN and LHA was detected by immunohistochemistry method. Results: Compared with the sham operation group, the ST-segment deviation, cardiac arrhythmia score and the expression of c-fos protein in the FN and LHA increased significantly in the model group (all P<0.05). Compared with the model group, the ST-segment deviation, cardiac arrhythmia score and the expression of c-fos protein in FN and LHA decreased significantly in the EA-Heart Meridian group (all P<0.05). Compared with the EA-Heart Meridian group, the ST-segment deviation and cardiac arrhythmia score increased significantly in the EA-Lung Meridian group, LHA+EA-Heart Meridian group and FN+EA-Heart Meridian group (all P<0.05); the expression of c-fos in FN increased significantly in the EA-Lung Meridian group and LHA+EA-Heart Meridian group (both P<0.05); the expression of c-fos in LHA increased significantly in the EA-Lung Meridian group and FN+EA-Heart Meridian group (both P<0.05). Conclusion: FN and LHA are involved in the mechanism of EA at Heart Meridian to improve the acute MIRI reactions, and the cerebellum may participate in the improvement of cardiac function by EA through the cerebellum-hypothalamus projection.