Objective To investigate the diagnostic value of acridine orange fluorescene(AO-F) in bladder cancers. Methods One thousand and sixteen bladder cancer patients were reviewed retro-spectively. The positive-rates of AO-F in different stages, grades, size, quantity, position of tumors, hematuria and treatment ways were evaluated. Results The total positive rate of AO-F was 78.05 % (793/1016). The positive-rate was 74.69% (611/818) in superficial stage and 91.92% (182/198) in invasive bladder cancer, 67.24% (351/522) in grade Ⅰ and Ⅱ , 90. 37% (413/457) in grade Ⅲ. The percentage of positive AO-F was 80.30% (750/934) in patients with hematuria, 52.44% (43/82) in patients without hematuria. The percentage was 79.87% (710/889) when the tumor size was more than 2 cm, 65.35% (83/127) when size less than 2 cm. 83.07% (363/437) sample was positive in multiple tumors, 74.27% (430/579) in single tumor. The percentage was 77.21% (105/136) in tumors involving trigone or neck of bladder, 78.07% (687/880) in tumors without involving these re-gions. There was 69.68% (393/564) in treatment with TURBt, 87.87% (268/305) in partial resec-tion, 91.74% (100/109) in total resection. A good association was observed between stage, grade, hematuria appearance, tumor size, quantity of carcinoma, treatment way and AO-F positive-rate, and a linear correlation was present between grade, stage and positive cytology. There was no significant association between position of the tumor and AO-F positive-rate. Conclusions The function of AO-F is significant in diagnosis of bladder cancer.

Objective To investigate the effects of constant magnetic field (CMF) on proliferation, apopto-sis and nitric oxide (NO) secretion of rat bone marrow-derived endothelial progenitor cells (EPCs) intervened by C-reactive protein (CRP). Methods EPCs were isolated from rat bone marrow by density gradient centrifugation and cultured on fibronectin-coated dishes. The cells were divided into five groups, i. e., control group, CRP (12 μg/ml) group, CRP plus CMF (0.1, 0. 5, 1.0 mT) groups. Samples were collected 24 hours after incubation. Cell proliferation was measured by MTT chromatometry. Apoptosis rate was detected by flow-cytometry. NO content of culture medium was measured by nitrate reductase method. Results As compared with control group, cell prolifer-ation in CRP group reduced significantly (0. 265±0. 008 vs 0. 316±0. 011, P < 0.05), NO secretion also de-creased significantly [(22.7±4.5) μmol/L vs (37.6±3.8) μmol/L, P < 0.05], cell apoptosis rate elevated sig-nificantly [(10.8±0. 8) % vs (4.2±0.5)% ,P < 0.05]. Cell proliferation in CRP plus 0. 5 mT or 1.0 mT CMF group (0. 295±0. 009,0. 302±0. 010) were much more than those in CRP group (P<0.05), NO secretion contents [(28.3±4.9) μmol/L, (29.2±5.6) μmol/L]were also much more than those in CRP group (P < 0.05) , apopto-sis rate [(7.4±0.5)% ,(6.9±0.6)%]was significantly lower than that in CRP group (P <0.05). Conclusion CMF at intensity of 0.5 mT and 1.0 mT can antagonize the effects of CR, promote proliferation of EPCs and secretion of NO and inhibit apoptosis rate of EPCs.

Objective:To systematically review the efficacy and safety of dexmedetomidine and midazolam in procedural sedation. Methods: PubMed,EMBase,Cochrane Library,CNKI,CBM and WanFang databases were retrieved to collect the randomized controlled trials (RCT) about comparion of efficacy and safety between dexmedetomidine and midazolam in procedural sedation up to March, 2017. Based on the inclusion criteria, the data extraction and quality evaluation were performed, and then the systematic evaluation was carried out.The outcome measures for efficacy were the satisfaction scores and pain scores of the patients and clinicians;the outcome measures for safety comparison were hypotension, hypoxia, and circulatory and respiratory complications.Results:There were 14 RCT satisfied the inclusion criteria including 949 patients.Compared with midazolam group, the incidence of pain, delirium, and analgesia of the patients in dexmedetomidine group had significant differences (P<0.05);but the incidence of respiratory depression, low blood pressure had no significant differences (P>0.05).Conclusion:When the adult patients are sedated, dexmedetomidine can be used as an ideal alternative to midazolam sedation.

In order to study neurotransmitter receptor regulation in the basal ganglia involved in the functional changes underlying levodopa-induced motor complications, quantitative autoradiography was used to observe receptor bindings of dopamine D1 and D2, N-methyl-D-aspartate (NMDA), amino-3-hydroxy-5-methylisoxazole propionic acid (AMPA) and amino butyric acid (GABA) in the basal ganglia of rats that had unilateral nigrostriatal lesions and had been chronically treated with levodopa until motor complications developed. The rats were randomly assigned to three groups: normal, denervated and treatment-complicated groups. The results showed that response duration to levodopa became progressively shorter and abnormal involuntary movement (AIM) score was progressively increased during the course of levodopa treatment. Chronic treatment augmented D1 receptors more than denervation, and reduced D2 receptors that were also increased by dopamine denervation. Striatal NMDA receptors were substantially up-regulated in the treatment-complicated group. Levodopa treatment did not change receptors of nigral AMPA, pallidal GABA, and subthalamic GABA, which remained the same as that in denervation group. However, chronic treatment reversed the increase of nigral GABA receptors caused by the lesion. It was concluded that a shortening of response duration and AIM mimicked levodopa-induced motor complications of Parkinson's patients. These data suggested that up-regulation of dopamine D1 and NMDA receptors in the striatum leads to an imbalance of stimulation through the striatal output pathways, which is associated with levodopa-induced motor complications.

Objective: To localize the neuroanatomical substrate of rapid eye movement sleep behavior disorder (RBD) and to investigate the neuroanatomical locational relationship between RBD and α-synucleinopathy neurodegenerative diseases. Materials and Methods: Using a systematic PubMed search, we identified 19 patients with lesions in different brain regions that caused RBD. First, lesion network mapping was applied to confirm whether the lesion locations causing RBD corresponded to a common brain network. Second, the literature-based RBD lesion network map was validated using neuroimaging findings and locations of brain pathologies at post-mortem in patients with idiopathic RBD (iRBD) who were identified by independent systematic literature search using PubMed. Finally, we assessed the locational relationship between the sites of pathological alterations at the preclinical stage in α-synucleinopathy neurodegenerative diseases and the brain network for RBD. Results: The lesion network mapping showed lesions causing RBD to be localized to a common brain network defined by connectivity to the pons (including the locus coeruleus, dorsal raphe nucleus, central superior nucleus, and ventrolateral periaqueductal gray), regardless of the lesion location. The positive regions in the pons were replicated by the neuroimaging findings in an independent group of patients with iRBD and it coincided with the reported pathological alterations at postmortem in patients with iRBD. Furthermore, all brain pathological sites at preclinical stages (Braak stages 1–2) in Parkinson’s disease (PD) and at brainstem Lewy body disease in dementia with Lewy bodies (DLB) were involved in the brain network identified for RBD. Conclusion The brain network defined by connectivity to positive pons regions might be the regulatory network loop inducing RBD in humans. In addition, our results suggested that the underlying cause of high phenoconversion rate from iRBD to neurodegenerative α-synucleinopathy might be pathological changes in the preclinical stage of α-synucleinopathy located at the regulatory network loop of RBD.

Objective To explore the changes of SOX9 and WT1 expressions in rat Sertoli cells irradiated by EMP ( electromagnetic pulse),S-HPM ( S-band high power microwave) and X-HPM ( Xband high power microwave).Methods Primary Sertoli cells were isolated from 3-week-old Wistar rats and its purity was immunocytochemistrically indentified with WT1.After exposure to 6 × 104 V/m EMP,100 mW/cm2 S-HPM and X-HPM for 4 min respectively,SOX9 and WT1 expressions in Sertoli cells were determined with real-time PCR and Western blot,respectively.Results SOX9 mRNA expression was decreased at 6 and 12 h post-irradiation of three different bands of electromagnetic microwave ( F =15.20and 4.84,P ＜ 0.05 ).SOX9 protein expression was also decreased at 6 and 24 h after irradiation ( F =8.46 and 7.47,P＜0.05).WT1 mRNA expression was decreased at6 and 12 h (F=13.46 and 5.08,P ＜ 0.05 ),but its protein expression was decreased only at 24 h post-irradiation ( F =10.26,P ＜ 0.05 ).Conclusions Three bands of electromagnetic radiation reduce the expressions of SOX9 and WT1 in rat Sertoli cells,which may provide molecular foundation for genital system hazards induced by microwave radiation.

The complete gene sequences of eight capripoxvirus strains in GenBank were aligned and analyzed with DNAStar software. We selected a size of 64 bp gene fragment that was located in gp064 region of goat pox virus (GPV) genome, and designed a pair of primers and a TaqMan-MGB probe against the gene fragment with Primer Express 2.0 software. Then, the fluorescence quantitative PCR (FQ-PCR) assay was developed and the standard curve of different dilution series was described. We extracted the DNA samples from clinical skin pox, scab and GPV infected materials of artificial challenge animals. The FQ-PCR assay has been performed for all kinds of DNA samples. The results showed that the FQ-PCR assay was sensitive, specific, stable and could be used for clinical diagnosis. This method provided an important tool for rapid diagnosis of goat pox clinically, and for study GPV pathogenesis in the course of disease occurrence, development and convalescence.
Animals ; Base Sequence ; Capripoxvirus ; genetics ; isolation & purification ; Goats ; Molecular Sequence Data ; Polymerase Chain Reaction ; methods ; Poxviridae Infections ; diagnosis ; virology ; Sensitivity and Specificity

In order to study neurotransmitter receptor regulation in the basal ganglia involved in the functional changes underlying levodopa-induced motor complications,quantitative autoradiography was used to observe receptor bindings of dopamine D1 and D2,N-methyl-D-aspartate (NMDA),amino-3-hydroxy-5-methylisoxazole propionic acid (AMPA) and amino butyric acid (GABA) in the basal ganglia of rats that had unilateral nigrostriatal lesions and had been chronically treated with levodopa until motor complications developed.The rats were randomly assigned to three groups:normal,denervated and treatment-complicated groups.The results showed that response duration to levodopa became progressively shorter and abnormal involuntary movement (AIM) score was progressively increased during the course of levodopa treatment.Chronic treatment augmented DI receptors more than denervation,and reduced D2 receptors that were also increased by dopamine denervation.Striatal NMDA receptors were substantially up-regulated in the treatment-complicated group.Levodopa treatment did not change receptors of nigral AMPA,pailidai GABA,and subthalamic GABA,which remained the same as that in denervation group.However,chronic treatment reversed the increase ofnigral GABA receptors caused by the lesion.It was concluded that a shortening of response duration and AIM mimicked levodopa-induced motor complications of Parkinson's patients.These data suggested that up-regulation of dopamine D1 and NMDA receptors in the striatum leads to an imbalance of stimulation through the striatal output pathways,which is associated with levodopa-induced motor complications.

Objective To investigate the effect of high power microwave(HPM) irradiation on neuropeptide Y (NPY) and neural nitric oxide synthase (nNOS) expression in the cerebral cortex and hippoeampus of Wistar rats. Methods A total of 110 Wistar rats were used for this study.Three groups of 30 Wistar rats were exposed to HPM irradiation at intensities of 3,10,30 and 100 mW/cm~2,respectively.Twenty rats served as controls and were ex- posed to sham HPM irradiation.At 6 h,and at 1,3,7,14 and 28 d after irradiation,five rats from each group were sacrificed,and their cerebral cortices and hippocampi were harvested.HE staining was used to highlight any change in the structure of the cerebral cortex or hippocampus.Immunohistochemistry techniques and image analysis were used to study the changes in NPY and nNOS expression.Results 10 to 100 mW/cm~2 HPM irradiation caused pyc- nosis and deep staining of some neurons in the cerebral cortex and hippocampus.The increase in nNOS expression and decrease in NPY expression observed were significant at 3 days after irradiation.Conclusion HPM irradiation can induce injury in neurons of the cerebral cortex and hippoeampus,and abnormal NPY and nNOS expression.

Objective:To evaluate the effect of zoledronic acid administration for osteoporotic vertebral compression fracture (OVCF) after treatment with percutaneous kyphoplasty (PKP).Methods:A retrospective case-control study was performed on 430 elderly patients with OVCF admitted to the Second Affiliated Hospital of Soochow University from January 2012 to December 2016. There were 31 males and 399 females, with age of 52-92 years[(72.8±8.3)years]. Fracture segments were at T 5-T 10 (82 vertebrae), T 11-L 2 (389 vertebrae) and L 3-L 5 (173 vertebrae). In zoledronic acid group ( n=178), patients were given zoledronic acid 3 days after PKP surgery. In basic treatment group ( n=252), patients were only given basic treatment after PKP surgery. Bone mineral density was measured before operation and one year after operation. Visual analogue scale (VAS) and Oswestry disability index (ODI) were assessed before operation, 3 days and one year after operation. Incidence rate of refracture, mortality and complication rate were recorded after operation. Results:All patients were followed up for 12-60 months (mean, 27 months). Before operation and at postoperative 1 year, the vertebral bone mineral density in zoledronic acid group was (-2.3±1.5)SD and (-1.2±2.3)SD ( P<0.05), and that in basic treatment group was (-2.2±1.2)SD and (-2.1±1.1)SD ( P>0.05). At postoperative 1 year, the bone mineral density in zoledronic acid group was significantly better than that in basic treatment group ( P<0.05). At preoperative 3 days, postoperative 3 days and postoperative 1 year, the VAS was (8.6±0.8)points, (2.8±0.8)points, (2.1±0.8)points in zoledronic acid group, and was (8.5±1.1)points, (2.9±0.9)points, (3.0±2.3)points in basal treatment group; ODI was 48.7±5.3, 24.0±2.9, 22.3±3.3 in zoledronic acid group, and was 48.3±6.1, 24.5±3.8, 27.6±4.0 respectively in basal treatment group. The VAS and ODI were significantly reduced in two groups at postoperative 3 days and 1 year compared to those before operation ( P<0.05). Moreover, the VAS and ODI in zoledronic acid group were significantly lower than those in basal treatment group at postoperative 1 year ( P<0.05). At postoperative 2 years, the incidence rate of refracture in zoledronic acid group was 10.1%(18/178), significantly lower than 16.7%(43/252) in basic treatment group ( P<0.05). Mortality rate in zoledronic acid group was 5.1%(9/178), and that in basic treatment group was 6.3%(16/252) ( P>0.05). No serious complications were observed in both groups such as nerve injury or pulmonary embolism. Conclusion:For OVCF patients, zoledronic acid given after PKP can improve the bone mineral density, reduce pain, fasten function recovery, and effectively decrease the refracture rate.