Objective To observe the clinical therapeutic effect of Capsule Long-Bi-Xiao(LBX) in treating benign prostatic hyperplasia(BPH).Methods 64 patients of deficiency of Qi and blood stasis type suffered with BPH were randomly divided into two groups.30 patients in the control group were treated with Capsule Long-Bi-Shu,while other 34 patients in the treated group were treated with LBX.Each group was observed for there months respectively.Results LBX decreased the international index of prostatic symptom(I-Pss) and the bother score(BS),improved the prostatic symptoms,raised the peak flow rate(Qmax) and the average flow rate(Qave),shrinked a portion of patients′ volume of prostate gland,reduced the volume of residual urine.After treatment,in the treated group,I-PSS and BS were reduced distinctly,and Qmax and Qave were heightened obviously,which was more effective than those in the control group.Conclusion LBX can achieve good action in the therapy of BPH by improving clinical symptoms,diminishing the volume of prostate and ameliorating the difficulty of urination.

The effects of polymerization conditions including scan potential range, scan cycles, the concentration ratio of template molecules to functional monomer, pH of the buffer, and washing time for removing the template molecule from the imprinted polymer on the difference of zero current potential of benzidine ( BZ) interaction with BZ-MIP were investigated. The optimum preparations were obtained. The imprinted capacity of benzidine, 4-chloroaniline, and 4-aminobiphenyl and carmine was calculated as 0. 632, 0. 1123, 0. 1123, 0. 0847 and 0. 0725, respectively. This indicated that BZ-MIP had good specific recognition and selectivity to benzidine, and other substances did not interfere with the binding of BZ-MIP with BZ. The zero current potential variation was linear with the lorgarithm of BZ concentration in the range of 4í10-8-1í10-5 mol/Lwith detection limitation of 1. 89í10-8 mol/L. The sensor was used to detect BZ in waste water sample with recoveries of 95 . 7%-104 . 2%.

ObjectiveTo investigate the effect of KN93,a CaMKII inhibitor,on the spinal NR2B expression in the bone cancer pain mouse and its underlying mechanism.MethodsThirty-six male C3IL/IIeJ mice were randomly divided into 3 groups:sham group( S,n =8 ),bone cancer pain group( BP,n =8 ) and KN93 group ( K,n=20).The mouse model of bone cancer pain was established by intra-femur inoculation of osteolytie NCTC 2472 cells in BP and K groups.At 14d post operation,mice in K group received intrathecal injection of 60nmol KN93/5μl in 20％ DMSO and mice in BP group and S group received 20％ DMSD 5μl respectively.Eight mice were selected randomly from each group at (1)d before inoculation,at 1 h before administration and at 1,2,4,24h after administration( T0-5 ) to be measured the paw withdrawal threshold(PWT) stimulated by von Frey filaments.Another 3 mice were sacrificed at the corresponding time point and the spinal cord L3 -5 were obtained for determination of NR2B expression by western blot.ResultsPWT was significantly decreased in group BP( (0.50 ± 0.11 ) g) and K( (0.52 ±0.10)g),except for group K at T3(P＞0.05),and NR2B cxpression up-regulated at T2-5 in BP( 1.78± 0.34),K groups ( ( 1.11 ± 0.14),(0.73 ± 0.03 ),( 1.11 ± 0.15 ),( 1.89 ± 0.32 ) ) compared with S group ( ( 1.78 ± 0.31 ) g,(0.33 ± 0.04),P ＜ 0.05 ).Compared with group BP,PWT was increased and NR2B expression down-regulated at T2-4 in group K.In contrast to T1,PWT at T2-4 upgraded in group K(P＜0.05 ),but no significant difference was observed in other groups (P＞ 0.05 ).ConclusionIntrathecal injection of KN93 can attenuate bone cancer pain in mice through inhibiting NR2B with a time-dependent manner and spinal CaMKII-NR2B pathway may participate in the development of bone cancer pain.

Objective To investigate effects of metabotropic glutamate receptor subtype 5 (mGluR5) antagonist MTEP on the nociceptive behavior and the expression of glial fibrillary acidic protein (GFAP) in spinal cord associated with bone cancer pain. Methods C3H/HeNCrlVr 60 male mice were randomly divided into 5 groups: ( 1 ) normal control group: the mice were given food and water ad libitum; ( 2 ) MTEP + Tumor group: the mice were treated by intrathecal gdministration ( once daily on the days 14 ～20 after inoculation of tumor cells)with MTEP (150 nmol); (3) physiological saline + Tumor group:the tumor mice were treated with the same volume of physiological saline; (4) MTEP + Sham group: the sham mice were treated with the same dose of MTEP;(5) physiological saline + Sham group: the sham mice were treated with the same volume of physiological saline.the mice pain behaviors were assessed with the paw withdrawal thermal latency (PWTL) at the corresponding time points, then the mice were killed and the samples of spinal cord were used to real-time PCR and western blot detection of GFAP mRNA and protein expression. Results The basic values of PWTL had no significant differences among all groups (P＜0.05). At day 14 after operation,no significant difference was found in the PWTL value between normal control group and the sham operation group. But in tumor group, the PWTL value was significantly lower than in the normal control group (P＜ 0.05 ). At day 21 after operation,the PWTL and the level of GFAP expression in the spinal cord had no significant differences among normal control group, MTEP + Sham group and physiological saline + Sham group (P ＞ 0.05 ); the PWTL ( (6. 18 ± 1.29 ) s) in physiological saline + Tumor group was significantly lower than in normal control group ( ( 15.91 ± 1.65 )s), physiological saline + Sham group ( ( 16.57 ± 1.86) s) and MTEP + Sham group ( ( 17.05 ± 2.43 ) s) (P ＜ 0.05 ), but the level of GFAP expression was higher than in the above three groups. In MTEP +Tumor group ,the PWTL (9.39 ± 1.94s) was higher than in physiological saline + Tumor group, and the level of GFAP expression was lower than in physiological saline +Tumor group (P ＜ 0.05 ). Conclusion Inhibiting spinal activation of astrocytes may be one of the MTEP anticancer pain mechanisms.

Objective To investigate the role of Ca2+/calmodulin-dependent protein kinase Ⅱ on pain behavior in a mouse model of bone cancer pain. Methods 40 male C3H/HeN mice were divided randomly into 5 groups:sham group (S group, n=8) ,control group (C group, n=8) and KN93 treat group (T1, n=8;T2, n=8;T3, n = 8 ). Group C and T were induced mouse models of bone cancer pain by intra-left-femur inoculations of osteolytic NCTC2472 cells while group S were injected only α-MEM. On the 14 d after inoculations,group S and C received intrathecal injection of 20% DMSO 5 μl . While group T1, T2, T3 received intrathecal injection of KN93 15nmol,30nmol,60nmol which dissolved in 5 μl 20% DMSO respectively. Mice received pain behavior tests including quantification of spontaneous flinches, paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) before and at 0.5 h,2 h,4 h,8 h after administration. Results Treatment with KN93(15 nmol) have no effect on bone cancer pain,while treatment with KN93(30 nmol,60 nmol) can dose-dependently reverse quantification of spontaneous flinches, mechanical allodynia and thermal hyperalgesia which were induced by bone cancer pain, At 0. 5h after administration, the quantification of spontaneous flinches of the two groups ( (7.25 + 1.49 ), (4. 12 + 1.36 ) ) were decreased when compared with control group ( 11.62 + 1.92 ),PWMT((1.28 +0.14)g;(1.75 +0.46)g),PWTL((14.64 +2.12) s; (16.85 + 1.61)s)were increased when compared with control group ( (0.47 + 0. 16) g, ( 11.32 + 1.68 ) s) (P ＜ 0.05 ＝. The effect lasts for at least 4 h and disappears at 8 h. Conclusion CaMK Ⅱ may play an important role in the mechanism of bone cancer pain. Intrathecal KN93 injection can effectively attenuated bone cancer pain.

Objective To investigate the infection of Mycoplasma in female urogenital system and the evolution of drug resistance. Methods Ureaplasma urealyticum (UU) and Mycoplasma hominis (MH) infections were examined by pathogen culture and fluorescence quantitative PCR in urogenital samples from 530 female patients in 2007, and drug sensitivity tests were performed in vitro. The results were compared with those in 2000. Results In 2000, there were 99 patients with Mycoplasma infections, in which 65 were of UU infections, 15 were of MH infections and 19 were of UU + MH infections. In 2007, there were 344 patients with Mycoplasma infections, in which 236 were of UU infections, 47 were of MH infections and 61 were of UU + MH infections. Patients aged 21～30 had the highest Mycoplasma infection rates both in 2000 (46.2%) and 2007 ( 50.5% ) ; while Mycoplasma infection rate in patients aged under 20 rose from 5.1% in 2000 to 12.8% in 2007 (χ2 = 4.682, P < 0.05). Both in 2000 and 2007, pathogens presented the highest drug resistance rates to tetracycline (TET) and erythromycin ( ERY ) which were all bore 80%. Compared with 2000, drug resistance rates to levofloxacin (LEV), azitromvcin (AZI) and ofloxacin (OFL) rose in 2007, and the differences were of statistical significance (P <0.05), while drug resistance rates to dmoxycycline (DOX), minocyclin (MIN) and josamycin (JOS) were still in the low level. Conclusions UU is the primary pathogen of infection in female urogenital system, and there is a tendency of Mycoplasma infection in younger age women. DOX, MIN and JOS can be the preferred medicines for Mycoplasma infections.

Glioma is a serious health threat for humans,so we urgently need to develop a more accurate,efficient and durable method to fight it.Immunotherapy is a fashionable treatment,which can stimulate the body's own immune system stimulation.And finding a reliable therapeutic target becomes the essential for glioma immunotherapy.The toll-like receptor 2 is form Ⅰ transmembrane receptor,which can be highly expressed in a variety of tumors and is closely linked to the aggressiveness and prognosis of the tumors.This article aims to explore the TLR2 expression and its association with tumors to provide new therapeutic targets for glioma immunotherapy.

Objective To evaluate the diagnostic value of transcranial doppler ultrasonography (TCD) for middle cerebral artery stenosis.Methods A comprehensive electronic search was performed in PubMed,EMBase,The Cochrane Library,CNKI,Wanfang Database and VIP Database to retrieve relevant studies on TCD in diagnosis of middle cerebral artery stenosis from initiation of the databases to January 2017.The general information and diagnostic parameters were documented from the retrieved studies.The quality of the prepared studies was evaluated by QUADAS-2 and the risk assessment maps brought by RevMan 5.3 statistical software.Pooled sensitivity,specificity,positive likelihood ratio (PLR),negative likelihood ratio (NLR) and the heterogeneity of the included studies were analyzed using the Stata 13.0 software.Summary receiver operating characteristic curve (SROC) was drawn and the area under the curve (AUC) was calculated.The publication bias was assessed with funnel plotting.Results A total of 11 studies were included for this Meta analysis,involving 2 550 patients.Heterogeneity test showed that the heterogeneity was established between studies in sensitivity,specificity,NLR and diagnostic odds ratio (DOR),resulting from disparity in study design and TCD test criteria (P＜0.05).Meta analysis revealed a pooled sensitivity of 0.88 (95％ CI:0.84～0.91),a specificity of 0.93 (95％ CI:0.91～0.95),a PLR of 12.93 (95％ CI:9.90～16.90),a NLR of 0.13 (95％ CI:0.09～0.17),a diagnostic score (SCORE) of 4.63 (95％ CI:4.32～4.94),a diagnostic odds ratio (DOR) of 102.64 (95％ CI:75.44～139.65),and an AUC of SROC of 0.96 (95％ CI:0.94～0.98).The sensitivity analysis after removing studies with sample capacity ＜100 showed that the confidence interval of the diagnostic parameters mostly overlapped with that of the original data.Conclusion As TCD shows good accuracy in diagnosing middle cerebral artery stenosis,it can be used in diagnostic screening of the disease.

DDX5 helicase (DEAD box helicases 5), also known as P68, is an important member of an ATP dependent RNA helicase.Studies have shown that DDX5 is abnormally expressed in a variety of cancers, targeting a variety of tumor related signal pathways, regulating upstream and downstream factors to affect the occurrence, invasion and migration of tumor cells. This article describes the biological role of DDX5 in malignant tumors and provides prospects for targeted treatment of tumors.

Objective To explore the relationship between Toll-like receptor 2(TLR2) and autophagy marker protein in glioma. Methods Glioma tumors of a total of 74 patients from June 2012 to December 2017 were surgically resected, including WHO gradeⅠtoⅡ32 cases, grade Ⅲ 20 cases, gradeⅣ22 cases. Immunohistochemistry and Western blot were used to detect the expression of TLR2, autophagy related protein LC3B, Beclin 1 and apoptosis related protein Bax and Bcl-2. The correlation between TLR2 and autophagy related protein LC3B and Beclin 1 were analyzed. Results In high grade glioma (HGG) tissue and low grade glioma (LGG) tissue, the TLR2 positive expression rates were 92.9％(39/42) and 75.0％(24/32), and there was significant difference (P<0.05). In HGG tissue, autophagy related protein LC3B, Beclin1 protein was strongly positive and the positive expression rates were 45.2％(19/42) and 52.4％(22/42). In LGG tissue, LC3B and Beclin1 protein positive expression rates were 18.8％(6/32) and 15.6％(5/32), and there were significant differences (P<0.05). Spearman correlation analysis showed that TLR2 protein was closely related to autophagy related protein LC3B (r=0.5638, P<0.05) and Beclin1 (r=0.6101, P<0.05). Conclusions TLR2 is highly expressed in HGG tissue, and its expression level may be related to autophagy, which has potential value as a targeted therapy.