Objective To investigate the effect of glutaminase 1(GLS1)specific inhibitor BPTES[bis-2-（5-phenylacetamido-1,3,4-thiadiazol-2-yl）ethyl sulfide]on the liver fibrosis in the mouse model of liver fibrosis induced by carbon tetrachloride(CCl4).Methods Male C57BL/6J mice were intraperitoneally injected with olive oil(control group),10%CCl4(10 μL/g,model group)or 10% CCl4(10 μL/g)+ BPTES(10 mg/kg,treatment group),with 10 mice in each group,two doses a week for four weeks to establish liver fibrosis model. Collagen deposition in mouse liver tissue was observed by Sirius red staining. The expression levels of actin alpha 2(Acta2),collagen typeⅠalpha 1(Col1a1)GLS1 and GLS1 protein were detected by qRT-PCR and immunohistochemical staining.Results Compared with the control group,the liver tissue of mice in the model group was generally enlarged,the surface was not smooth and granular,and the ratio of liver mass to tibia length significantly increased(t = 2. 979,P < 0. 05);The Sirius red positive area of collagen deposition increased signifi-cantly in the liver tissue of mice in the model group(t = 7. 661,P < 0. 01),the relative expression levels of Acta2 and Col1a1 significantly increased(t = 4. 335 and 5. 319,respectively,each P < 0. 01),and the mRNA and protein levels of GLS1 significantly increased(t = 5. 319 and 9. 725,respectively,each P < 0. 01). However,compared with the model group,the BPTES treatment group had a reduction in liver mass,a significant reduction in the Sirius red positive area of collagen deposition in liver tissue(t = 7. 427,P < 0. 01),and a significant reduction in the relative expressions of Atca2 and Col1a1(t = 3. 713 and 2. 628,respectively,each P < 0. 05).Conclusion Inhibition of GLS1activity can significantly improve the degree of liver fibrosis induced by CCl4,providing a new idea for the treatment of liver fibrosis.

Objective To evaluate the clinical effect of ultrasound-guided botulinum toxin A (BTX-A)injection for upper limb spasticity in children with cerebral palsy.Methods Twenty children with upper limb spasticity resulting from cerebral palsy were divided equally into a BTX-A injection group and a control group. Both groups received standard rehabilitation treatment. For the injection group, color ultrasonography was used to guide the accurate injection of BTX-A into the spastic muscles of the arm. They received rehabilitation training the day after the injection. For all patients, muscle spasticity and upper limb movement and function were evaluated before treatment and 1, 2, 4, 8 and 12 weeks later using a modified Ashworth scale and the Fugl-Meyer assessment.Results After two weeks of treatment, muscle spasticity and upper limb movement and function in the injection group were significantly better than before the injection.The improvement in muscle spasticity was greatest two weeks after the injection. The average therapeutic effect in the injection group was significantly better than among the controls.Conclusion BTX-A injection under ultrasound guidance helps relieve upper limb spasticity in cerebral palsy. It has the advantages of accurate localization and safety and gives superior results compared to rehabilitation treatment alone.

Humans ; Hypersensitivity

Objective To study nitric oxide (NO) and nitric oxide synthase (NOS) in brain and myocar-dium of depression model rats and to explore the mechanism of brain and myocardium injuryed. Methods The de-pression model rats were produced by chronic mild unpredictable stress and separation. The behavior of rats were detected by open field test and sucrose consumption test. The contents of NO and NOS were determined with spec-trophotometric method. Results Compared with the normal control, the contents of NO [Brain ( 8.97±2.22 )μmol/g prot vs ( 1.86±1.28 )μmol/g prot; Myocardium (9.67±1.53) μmol/g prot vs (2.67±1.08)μmol/g prot] and NOS[Brain(9. 50±1.89) U/mg prot vs (2.31±0. 97) U/mg prot; Myocardium( 11.20±1.47) U/mg prot vs(2.53±0.97)U/mg prot] in brain and myocardium were significantly increased (P<0.01)of depression model rats. Conclusion The contents of NO and NOS increase significantly in brain and myocardi-um of depression model rats and it may induce the injury on brain and myecardium of them.

OBJECTIVE: To investigate therapeutic progress of cerebral intravascular stent, and to evaluate biocompatlbility with host.METHODS: Articles were collected from CNKI and Medline database with the keywords of "cerebrovascular disease, stent, and therapy" in both Chinese and English from 1989 to 2009. Among 53 articles, 22 were included according to inclusion and exclusion criteria; while the included articles were summarized in the fields of therapeutic progress of cerebral intravascular stent,complication following cerebral intravascular stent implantation, and biocompatlbility of cerebral intravascular stent in order to investigate the biocompatibility of various stents.RESULTS: Cerebral intravascular stent was mainly used to treat cerebral artery stenosis, cerebral aneurysm, venous sinus stenosis, and thrombus. Complications following cerebral intravascular stent implantation included carotid sinus syndrome,hypertransfusion syndrome, cerebral angiospasm, thrombosis, and restenosis. Pre-enlargement prior to implantation in the stenotic region played an important role in avoiding deformation and displacement of stent. Restenosis correlated to stent types following cerebral intravascular stent implantation. For example, metal stent could promote thrombosis; however, polymer which had an excellent biocompatibility to vessel wall was superior to metal stent, thus it could prevent endomembrane proliferation following implantation. Metal-coated stent could inhibit aggregation of platelet; additionally, drug stent could effectively prevent restenosis via high-concentration drug release for a long term.CONCLUSION: Cerebral intravascular stent is considered as an ideal tool to treat cerebrovascular disease. Metal stent has a poor compatibility, but polymer stent, coating stent, and drug stent have a good compatibility.

Objective To study the relationship between the gene mutations of DNA gyrase subunit A(gyrA)and quinolone resistance in Salmonella typhi. Methods The genes of gyrA DNA of Salmonella typhi S275(a clinically isolated quinolone susceptible strain)and its spontaneous quinolone-re-sistant mutant RGl were examined in this study with polymerase chain reaction(PCR),restrictive frag-ments length polymorphism(RFLP),single strand conformational polymorphism(SSCP)and nucleotide sequencing. Results Nudeotide sequencing of gyrA in Salmonella typhi S275 revealed that the bases of 128～426 kept highly conservative as compared with those of Escherichia coli KL-16,with only 7.49%difference in the gyrA nucleotides 128～426 between the two strains.Most of the mutations were silent mutations,which contributed to 3 amino acid substitutions in gyrase(including Thr-45→His,Arg-49→Leu and Val-56→Gly),and all these substitutions were located outside the quinolone resistance determining re-gion(amino acids 67-106 of subunit A of gyrase).In comparison with Salmonella typhi S275,a single mutation was found at base 247 of gyrA of Salmonella typhi RG1,with change transferred from T to G and led to a substitution of Ser-83→Ala.The mutation might be responsible for the increase of MICs of nalidixic acid,ofloxacin and ciprofloxacin against Salmonella typhi from 2,0.06 and<0.03 to 512,2,and 1 mg/L respectively.Ser-83→A1a was also a newly discovered substitution in gyrA of Salmonella spp.The results of PCR-RFLP and SSCP were in concordance with results of nucleotide sequencing. Conclu.sions The mutation of gyrase at the 83rd amino acid maybe play a principal role in the resistance of Salmonella typhi to quinolone.

Circulating endothelial cells (CEC) are endothelial cells which are detected in the peripheral blood. There are very few CEC in healthy adults while the number is obviously increasing in patients with arthrosclerosis, diabetes mellitus, lupus erythematosus, et al. Nowadays, flow cytometry analysis and immunomagnetic isolation for CEC are employed successfully in clinic and scientific research. Several research findings have confirmed that there is intimate relation between CEC and tumorigenesis. Because of the important role in angiogenesis and tumor growth, CEC would be a perspective tumor marker in antiangiogenesis and would also predict the chemotherapy efficacy.

Today,more and more patients with diabetes are requiring surgical intervention.Not only the metabolic disturbance of carbohydrate will be aggravated by surgical stress,but also the risk of perioperative complications and mortality have been greatly increased in patients with diabetes.Therefore,a complete preoperative assessment and blood glucose management of preoperative,intraoperative,and postoperative periods are needed to get full assurance for diabetic patients to undergo surgery and to pass through the perioperative period smoothly.

BACKGROUND: Peroxisome proliferator-activated receptor-gamma(PPAR-γ) can restrain the inflammatory reaction of hypertrophic myocardium through restraining the expression of interleukin-6, cyclooxygenase, endothelin-1, nitricoxide synthase, matrix metalIoproteinase-9, gelatinase and adhesion molecule, etc.OBJECTIVE: To observe the influence of rosiglitazone sodium(the ligand for PPAR-γ) on inflammatory factors in rats with myocardial hypertrophy in the course of myocardial hypertrophy resulting from pressure load.DESIGN: Randomized controlled trial based on animals.SETTING: Department of Cardiovascular Surgery, Xinqiao Affiliated Hospital, the Third Military Medical University of Chinese PLA.MATERIALS: Fifty purebred male SD rats of S.P.F. Grade, whose body mass was (220±22) g.METHODS: The experiment was completed in the Institute of Battle Surgical Research, the Third Military Medical University of Chinese PLA from August 2004 to October 2005. Fifty rats were randomly divided into 5groups: control group, sham operation-normal saline group, sham operationrosiglitazone group, myocardial hypertrophy-normal saline group and myocardial hypertrophy-rosiglitazone group, 10 rats per group. The rat model of myocardial hypertrophy induced by pressure overload was established with the method of coarctation of abdominal aorta. Rosiglitazone group: At the postoperative 4th week, the rats were injected intraperitoneally with the Normal saline group: At the postoperative 4th week, the rats were injected intraperitoneally with normal saline[1 mL/(kg.d)] for 1 week. At the postoperative 5th week, the indexes of myocardial hypertrophy and hemodynamics were determined. The contents of tumor necrosis factor-α, platelet activating factor and myeloperoxidase in the left ventricle muscle were determined with radioimmunosorbent technique. The expression of PPAR-γ mRNA was detected with RT-polymerase chain reaction. The activity of nuclear factor-κB was detected with EMSA.MAIN OUTCOME MEASURES: The indexes of hemodynamics, cardiac ventricle reconstitution and cardiac muscle in the rat models.RESULTS: Except 1 rat in the control group died of the external injury induced by biting after 3 weeks, 49 of 50 rats entered the result analysis.①After the coarctation of aorta, the contents of tumor necrosis factor-α, platelet activating factor and myeloperoxidase of hypertrophic myocardium in the myocardial hypertrophy-rosiglitazone group were lower significantly than those in the myocardial hypertrophy-normal saline group(P ＜ 0.01-0.05), but they were still higher than those in the control group(P＜0.01).②The expressions of PPAR-γ mRNA of myocardial tissue in both the myocardial hypertrophy-rosiglitazone and myocardial hypertrophy-normal saline groups were higher obviously than those in the control group(P＜0.01), and those in the myocardial hypertrophy-rosiglitazone group were higher than those in the myocardial hypertrophy-normal saline group(P＜0.01).③The activity of nuclear factor-κB combined with DNA in cardiac muscle cell in both the myocardial hypertrophy-normal saline and myocardial hypertrophy-rosiglitazone groups were higher obviously than those in the control group (P＜0.01), and those in the myocardial hypertrophy-rosiglitazone group were lower obviously than those in the myocardial hypertrophy-normal saline group(P＜0.01).CONCLUSION: The increasing of pressure load induces myocardial hy pertrophy. The activation of nuclear factor-κB in the tissue of hypertrophic myocardium is strengthened obviously. The expressions of tumor necrosis factor-α, platelet activating factor and myeloperoxidase in hypertrophic myocardium increase. This inflammatory reaction, which is strengthened obviously, can be restrained by rosiglitazone sodium that is the synthetical lig and for PPAR-γ.

China ; Hospital Design and Construction ; standards ; Hospitals ; Humans ; Occupational Exposure ; analysis ; prevention & control ; Radiology Department, Hospital ; Safety ; standards