The imbalance in the fibrinolytic system participates in the pathophysic-logical processes of ischemic stroke. Most researchers consider that the fibrinolytic activity decreases in patients with ischemic stroke, while others believe that it increases. Mild hypothermia is a therapeutic approach with great potential and plays the neuroprotective effect through a variety of mechanisms. Animal experiments have demonstrated that the treatment with mild hypothermia may increase the plasma fibrinolytic activity and decrease the expression of local plasminogen activator in ischemic area. Howere, the related clinical research studies are few, and most of them are limited in the safty and collaborative research of mild hypothermia combined with other treatment therapies.

Objective To investigate the effect of mild hypothermia therapy on plasma tissue-type plasminogen activator (tPA)/plasminogen activator inhibitor-1 (PAI-1) in patients with massive cerebral infarction (MCI).Methods The patients with MCI were randomly divided into the conventional therapy group and the mild hypothermia therapy group.On the basis of conventional therapy,the latter received local mild hypothermia therapy for 48 hours immediately after admission.Enzyme-linked immunosorbent assay was used to detect plasma tPA and PAI-1 at admission and at 48 hours after mild hypothermia,respectively.The general information and the tPA and PAI-1 levels before and after treatment in both groups were compared.Results A total of 46 patients with MCI were included.There were 26 and 20 patients in the conventional therapy group and the mild hypothermia therapy group,respectively.There were no significant differences in the general information,the tPA and PAI-1 levels before and after treatment in both groups,and the levels of plasma tPA (80.98 ± 34.64 pg/mL vs.110.1 ± 32.7 pg/mL; t =3.462,P =0.013) and PAI-1 (145.40 ± 45.29 pg/mL vs.174.2 ± 38.0 pg/mL; t =4.854,P =0.034) at 48 hours of mild hypothermia therapy in the mild hypothermia therapy group were significantly lower than those in the conventional therapy group.Conclusions Mild hypothermia therapy may decrease the plasma tPA and PAI-1 levels in patients with MCI,and it may be associated with the neuroprotective effect of hypothermia therapy.

Objective: To improve the standardization method for ethanol potassium hydroxide volumetric solution. Methods: A new potentiometric titration method was established and compared with the indicator method described in Chinese Pharmacopeia (2010 edition) . Results:There was no significant difference between the results of the potentiometric method and the indicator method( P>0. 05). Furthermore, the potentiometric titration had significant jump range, good precision and high reliability. Conclusion:The po-tentiometric method can be used in the standardization of ethanol potassium hydroxide volumetric solution.

Objective To develop a double antibody sandwich ELISA for quantitatively detecting Japanese encephalitis virus(JEV) antigen.Methods The anti-JEV polyclonal antibodies were used to coat ELISA plates.Anti-JEV monoclonal antibodies were used as enzyme-labeled conjugate.A standard curve based on known amounts of JEP antigen was established by the ELISA.Various parameters of the assay were analyzed.Results The optimal linear range was 12.5～200 U/ml(r=0.9989).The quantitation limit was 12.5 U/ml.The recovery rate for the accuracy test was 85.0%～103.3%.The coefficients of variation for intra-assay and inter-assay precision were 4.3%and 5.5%respectively.No cross-reaction was observed with HAV vaccine,influenza vaccine,Vero cell Iysates,newborn bovine serum,or human albumin.Conclusions The data indicate that the ELISA developed in this study has high specificity,precision, accuracy,and stability.The assay should be suitable for quantitative determination of JEV antigen in various vaccine products.

OBJECTIVE: To prove that the neural stem cell can be separated from neural tissue in adult mammalian. Stem cells can separate and proliferate continually, and can divide further into neuron and glial cell. The uptodate researches of neural stem cells suggest a prospective approach to treat neurological diseases, i.e. the dysfunctional cells may be replaced with neural stem cells by transplantation for functional reconstruction. Therefore,many kinds of directional differentiative signal controlling of neural stem cells to differentiate at a certain direction.DATA SOURCES: Using the key term neural stem cell, differentiation,signal and cell transplantation, we searched the MEDLINE database plus the relevant articles in English language from January 1995 to August 2004. Meanwhile, using the key terms mentioned above, we searched Chinese journal full-text database, Wanfang database in Chinese language from January 1995 to August 2004.STUDY SELECTION: The articles on extracellular signal of the differentiation of neural stem cell with full summarization were selected.DATA EXTRACTION: A total of 30 articles were eligible, and the relevant contents were compared and summarized. Eighteen articles were selected at last.DATA SYNTHESIS: All 18 articles contained different aspects of signal regulation of neural stem cell, including various key cellular factors and autogene regulation.CONCLUSION: Both cellular signals in vivo and in vitro can affect the cell differentiation. The vital problem to be solved is how to induce neural stem cells to differentiate at a certain direction so as to realize the aim of transplantation.

Objective To explore the production of medical polypropylene anti-bacterial mesh coated with triclosan,and study the properties of its controlled-release drugs,as well as the efficiency of the mesh coated with triclosan.Methods A medical polypropylene anti-bacterial mesh coated with triclosan was produced by the method of solvent evaporation,with triclosan as antibacterial agent and ethylene-vinyl alcohol copolymer as carrier.The meshes were divided into four groups: A,B,C and D.The meshes in A,B and C(experimental) groups were coated with triclosan,and D group was control group.The ultrastructure of meshes of the 4 groups was observed under electron microscope.The slip diffusion method was used to observe the diameter of bacteriostasis-rings in different time periods.At the same time,we observed the maximum tensile strength of the mesh in transverse and longitudinal axis when they were pulled off before and after the experiment.Results The surfaces of B group were uniform and smooth,and the coating could continuously release drugs during 7 days in sodium chloride.The diameter of bacteriostasis-rings in B group was significantly larger than that in control group(P

5cm and with metastasis of lymph nodes than that in the ones of well-or(mild-differentiation),filtration of only muscular layer by cancer cells,maximal diameter of mass

Objective To evaluate the changes in the expression of neuron-restrictive silencer factor (NRSF) in the spinal cord of mice with bone cancer pain.Methods Forty-eight pathogen-free adult male C3H/HeJ mice,aged 4-6 weeks,weighing 20-25 g,were randomly divided into 2 groups (n=24 each) using a random number table:sham operation group (group S) and bone cancer pain group (group BCP).Bone cancer pain was induced by injecting 2× 105 NCTC2472 osteolytic sarcoma cells in α minimal essential medium into the medullary cavity of the right distal femur in group BCP.Only α minimal essential medium was injected into the medullary cavity of the right distal femur in group S.The mechanical and thermal pain thresholds were measured on 5,7,10 and 14 days after inoculation (T1-4).Six mice in each group were randomly selected after measurement of pain thresholds at T1-4 and sacrificed,and the lumbar enlargement segments of the spinal cord were harvested to detect the expression of NRSF.Results Compared with group S,the mechanical pain threshold at T2-4 and thermal pain threshold at T3.4 were significantly decreased,and the expression of NRSF was significantly down-regulated at T1-4 in group BCP (P＜0.05).Conclusion The mechanism underlying the development of bone cancer pain is probably related to down-regulation of NRSF expression in the spinal cord of mice.

As a neuroprotective measure,the application and research of mild hypothermia in clinical practice have been very extensive.Using mild hypothermia has achieved a positive efficacy in many diseases,such as brain damage after cardiac arrest and neonatal hypoxic-ischemic encephalopathy,etc.Although mild hypothermia has a large number of animal experiments and clinical studies in the treatment of ischemic stroke,and animal experiments have confirmed that it has the exact neuroprotective effect,the neuroprotective effect of mild hypothermia in the treatment of ischemic stroke has not yet come to a unified conclusion in the clinical studies.Its clinical efficacy does not seem to be as optimistic as expected.Therefore,it is necessary to analyze the transforming problems of mild hypothermia for treatment of ischemic stroke from animal experiments to clinical practice,and to provide ideas for the clinical application of mild hypothermia for treatment of ischemic stroke.

Objective To explore the role of tissue-type plasminogen activator(tPA) in neonatal rat with hypoxia-ischemia brain damage(HIBD).Methods Seven-day-old Wistar rat pups were used for the Vannucci model of HIBD.Reverse transcription-polymerase chain reaction(RT-PCR),terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL),double immunostaining and immunoblot analysis were adapted to determin the expression of tPA at acute phase after HIBD and neural cell apoptosis and the blood-brain-barrier(BBB) damage.Results Neonatal hypoxia-ischemia triggers persistent induction of the plasminogen system.The increase of tPA activity induced the degradation of laminin and occludin which would aggravate the BBB damage.The number of neural cell apoptosis after HIBD increased progressively with the reperfusion time.Conclusions The increase of tPA at the acute phase after HIBD can help clot to dissolve,while its extravascular proteolysis will induce cell apoptosis and BBB damage which will aggravate brain injury.