OBJECTIVE:To evaluate the safety of various high polymer biomaterials to prevent tendon adhesion,and analyze whether the improvement of injured degree,toxic and side effects,and slipping function of tendon can influence tendon healing.METHODS:A computer-based online search of CNKI was undertaken to identify randomized controlled articles about the effect of various high polymer biomaterials on tendon adhesion with the keywords of "tendon adhesion,biomaterials,and barrier" from 1990 to 2005.Retrieval data were then extracted and analyzed.RESULTS:Among 11 tests,there were 571 patients with tendon injury and 7 animal models with tendon injury,according to inclusion criteria.After surgery,high polymer biomaterials were used to prevent from adhesion and reduce exogenous adhesion incidence.Following-up results demonstrated that high polymer biomaterials which affected endogenous and exogenous healing of tendon might prevent from tendon adhesion,provide foundation for early controlling passive activity,reduce exogenous adhesion occurrence,improve moving function of tendon,and promote tendon healing.CONCLUSION:Barrier effect of high polymer biomaterials can well prevent from tendon adhesion in clinic,especially intrathecal injection or local injection of sodium hyaluronate has both trophic and lubricant actions in preventing from tendon adhesion.However,other effective indicators and safety need to be further studied due to less including tests and weak evidences.

BACKGROUND: With wide application of biotechnological substitute materials, pelvic repair and reconstruction develop to a certain degree. Biomaterial patch is a major substitute for repairing injured pelvic fascia tissue, so it is widely used for pelvic reconstruction.OBJECTIVE: To investigate the feasibility, efficacy, and clinical value of biomaterial patch to pelvic reconstruction in the females.METHODS: Articles related to pelvic functional disorder, pelvic reconstruction, and application of patch implant were retrieved from PubMed (http://www.ncbi.nlm.nih.gov/PubMed) and (http://www.wanfangdata.com.cn) with the key words of "reconstruction of whole pelvic floor, mesh, synthetic mesh implants" in both Chinese and English between 1990 and 2008. Duplication studies were excluded. A total of 54 articles were initially retrieved, and 17 ones were included in the final analysis.RESULTS AND CONCLUSION:Pelvic organ prohpse, which was a major symptom of pelvic disorder in the females, caused by defect of pelvic supporting structure, injury, and functional disorder. Traditional operation could not solve fundamental question.At present, substitute materials for pelvic repair and reconstruction mainly include biomaterial patch (self-substitute materials, homogeneity substitute materials, and heterogeneity substitute materials) and artificial patch. All of them could substitute the injured pelvic fascia tissue; therefore, they were major substitute materials of pelvic tissue and widely used for pelvic reconstruction. Patch which was used for pelvic reconstruction realized the recovery of anatomic structure and caused functional recovery, with simple and easy processing. Additionally, patch application did not prolong operative time and cause complication, but induced well tolerance, security and reliability, and remarkable short-term effect on patients. However, the long-term efficacy should be further studied. The modified pelvic reconstruction is clinically valuable for patients with varying prolapsed sites.

Objective To study the neurotoxic effects of acute exposure of methylmercury at low dose and to provide some experimental data for deeply exploring the early mechanism of neurotoxicity of methylmercury. Methods SD rats were administered with methylmercury chloride by intraperitoneal injection with different doses of 0.05, 0.50 and 5.00 mg/kg and different exposure times of 20 min, 1 h, 4 h, 24 h. Mercury, ACh and AChE contents in rat brains were measured. Results Mercury contents in rat brains significantly increased after 20 min-exposure at both 0.50 and 5.00 mg/kg doses. Significant increase occurred after 4 h exposure at dose of 0.05 mg/kg. ACh and AChE in rat brains significantly changed after 20 min at every dose, showing certain dose-response and time-response relations. Conclusion Changes of ACh and AChE in rat brain after administration of low dose(0.05 mg/kg) and short time(20 min) exposure suggested certain modulation of CNS had been initiated. With the increases of exposure dose and time, methylmercury might begin to accumulate in rat brain and induce the significant changes of ACh and AChE.

OBJECTIVE:To provide reference for the further standardization of biological products injection for treatment in-structions. METHODS:32 biological products injection for treatment instructions collected from Ma’anshan Center for Disease Control and Prevention and Ma’anshan Central Hospital during Jan. to Jun. in 2015. The information of marked item was summa-rized and analyzed. RESULTS & CONCLUSIONS:Among 32 biological products injection for treatment instructions, the mark rates of drug names,main ingredients,character,indications,specification,usage and dosage,package,term of validity,opera-tive norm,license number,manufacturing enterprise and other items all reached 100%. Although the mark rates of ADR,contrain-dication,precaution,drug use of pregnant women and nursing mothers,drug interactions,pharmacokinetics,drug use of the elder-ly,storage and other items were relatively high,but some items lacked the specific description of the content. The mark rates of drug use of children,drug overdose,toxicology,warnings,clinical trial were 56.25%,62.50%,59.38%,37.50% and 18.75%. Some biological products injection for treatment instructions are not revised timely and not complete in content and non-standard in writing,which can not meet the needs that clinical pharmacists and patients get enough drug safety information from instructions. Manufacturing enterprise is suggested to label the content of package inserts completely,verify and supplement related content, standardize and improve the instructions.

The work aims to study the drug metabolizing enzymes involved in the metabolism of butylphthalide and evaluate the induction and inhibition activities of butylphthalide on CYP450 isoenzymes by using in vitro (liver microsome incubation system of rats and human) and in vivo (CYP induced model of rats) method. Butylphthalide was incubated with selective inhibitors of CYP450, and its metabolic rate was determined to identify the metabolizing isoenzymes of NBP in rat (normal and induced rats) and human liver microsomes. The in vitro inhibition effect of butylphthalide on 6 main liver microsomal CYP450 isoenzymes was evaluated by using probe drugs; the induction and inhibition activities in vivo of butylphthalide on CYP450 isoenzymes were evaluated by NBP ig dosing (160 mg x kg(-1)) and iv dosing (20 mg x kg(-1)) in rats. After adding the specific inhibitors of CYP2C11, 2E1 and 3A 1/2 for rat, CYP2C19, 2E1 and 3A4/5 for human, the metabolism of NBP in rat and human liver microsomes were reduced 38.8%, 86.2%, 78.4% and 51.0%, 92.0%, 58.9% of control, respectively. The metabolic rates of NBP in CYP2E1 and 3A 1/2 induced rat liver microsomes were increased 25.5% and 68.9%. High concentration of NBP (≥ 200 μmol x L(-1), in vitro) could inhibit the activities of CYP1A2, 2C6, 2C11 and 2D2 in rats, and high concentration of NBP ( ≥ 15 μmol x L(-1), in vitro) could inhibit the activity of CYP2C19 in human. All the results indicated that NBP should be mainly metabolized by CYP2E1, 2C11 and 3A 1/2 in rats and CYP2E1, 2C19 and 3A4/5 in human. High concentration of NBP could inhibit human CYP2C19 in vitro. No significant induction/inhibition effects of NBP were observed on rat liver CYP450 isoforms after ig 160 mg x kg(-1) NBP or iv 20 mg x kg(-1) NBP.

Objective To test experimentally Fluoro-Jade B(FJB) stain method for detecting degeneration of neurons in the basal ganglia. Methods Kainic acid(KA)-lesion model by stereotaxical injection of KA into striatum of rats,MPTP-lesion model by injection of MPTP into intraperitoneal cavity of mice,as well as KA-lesion model of cultured striatal cells were firstly prepared.FJB stain dye was then used to visualize degeneration of neurons in above KA-or MPTP-lesion models. Results KA-or MPTP-induced degenerative neurons including cell bodies and processes could be clearly visualized by FJB stain dye.In the brain sections,FJB-positive stained degenerative neurons were numerously observed in the striatum of KA-lesion rats and the substantia nigra pars compacta of MPTP-treated mice,but not detected in the control animals.Moreover,degenerative neurons were also detected with FJB stain in cultured striatal neurons.Semi-quantitative analysis on percentage(?s) of FJB-positive neurons constituting total cultured striatal neurons in unit area showed that degenerative neurons of KA-lesion group (8.42?1.09)% was evidently more than that of controls (3.42?0.45)%,P

rAdinbitor was cloned from Gloydius blomhoffi brevicaudus in the laboratory. Previous researches had proved that rAdinbitor could inhibit proliferation of C6 glioma cells as well as promote their apoptosis. The molecular mechanism of rAdinbitor’s effects on C6 cells need to be further studied. rAdinbitor was expressed in E. coli BL21/pET23b-adinbitor and purified with Ni Sepharose 6 Fast Flow. The purified protein was confirmed by Western blotting. C6 cells were induced with fibronectin (FN). The effects of rAdinbitor with different concentrations on the expression of FAK, MEK1/2 and Caspase-3 as well as on activity of FAK and ERK1/2 in FN-induced C6 cells were studied by immunoblotting and immunoprecipitation. Results showed that rAdinbitor with different concentrations could obviously reduce the expression of FAK and MEK1/2, increase the expression of Caspase-3, as well as decrease ERK1/2 phosphorylation; besides 10 mg/L rAdinbitor, other concentrations’ rAdinbitor could inhibit FAK phosphorylation obviously. All those effects were dose-dependent. Results indicate that the effects of rAdinbitor on decreasing expression and activity of FAK and inhibiting Ras-MAPK signaling pathway play an important role in suppressing the proliferation of C6. Furthermore, the increase in Caspase-3 expression implies that the increase in apoptosis of C6 cells might be due to the suppression of rAdinbitor on the activity of ILK and PI-3K/Akt pathway.

Objective To investigate the effects of celastrol on the expressions of macrophage migration inhibitory factor(MIF)and matrix metalloproteinase-9(MMP-9)in the aorta of apoE gene knockout mice with earlier atherosclerosis.Methods Eight-week-old ApoE gene knockout male mice were divided randomly into control group and celastrol treatment group(n=6 in each group).The mice in celastrol group were given.celastrol(2 mg?kg-1?d-1)by intraperitoneal injection for 4 weeks;and the mice in control group were only given equivalent amount of dimethyl sulfoxide(DMSO).HE staining of root aorta were used to observe the histomorphological changes and measure the size of plaque in ApoE-/-mice.The expressions of MIF and MMP-9 were detected by immunological histochemical method.Results The area of lipid plaque in the mice treated with celastrol was significantly smaller than that of the control(P

Aim To explore the inhibitory effect of dexamethasone on the expression of SH2-B? in the lung and the visceral sensory afferent system(C7-T5 spinal ganglia and the corresponding posterior horn of the spinal cord)of asthmatic mice.Methods Murine model of asthma of BABL/c mice was induced by ovalbumin in vivo.By means of immunohistochemistry and Western blot,the expression of SH2-B? in the lung,C7-T5 spinal ganglia and corresponding spinal cord was detected and the inhibitory effect of dexamethasone on it was observed.Inspiratory airway resistance was measured with AniRes 2003 lung function system.Results The expression of SH2-B? in the lung,C7-T5 spinal ganglia and the corresponding spinal cord of the asthmatic mice was much higher than that of the control group and the dexamethasone group(P

The rat single-pass intestinal perfusion model was applied to study the effect of CYP3A and P-glycoprotein on the absorption of buagafuran in lumen of rats. Buagafuran concentrations in intestinal perfusate and blood in vena mesenterica collected at different time points after perfusion were determined by GC-MS. Permeability coefficient of buagafuran was calculated by the equation [P(lumen) = -(Q/2pirl)Ln(C(out)/C(in)) and P(blood) = (deltaM(B)/deltat)/(2pirl)]. The effects of troleandomycin (TAO, CYP3A inhibitor), cyclosporin A (CYP3A/p-glycoprotein inhibitor) on the absorption of buagafuran in lumen were observed. After rat single-pass intestinal perfusion, the cumulative amount of buagafuran in mesenteric vein of rat was 73.4, 82.9, and 98.3 pmol x cm(-2) and were increased 3.9, 4.6, and 5.6 fold by addition of inhibitor of P-gp (LSN335984), CYP3A (TAO) or P-gp and CYP3A (CsA), respectively. Moreover, the metabolized fraction of buagafuran was decreased by 12%, 11% and 21% with inhibitors. The results suggested that the poor bioavailability of buagafuran was mostly due to the interplay of P-gp and CYP3A on the absorption, transport and metabolism of buagafuran in intestine of rats.