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.

Granulocyte-Macrophage Colony-Stimulating Factor ; therapeutic use ; Humans ; Recombinant Fusion Proteins ; therapeutic use

Antiphospholipid Syndrome ; diagnosis ; etiology ; therapy ; Child ; Humans ; Lupus Erythematosus, Systemic ; complications ; Male

Objective To explore the effect of progesterone on the rate of neuronal apoptosis and nitric oxide(NO) level in the cortex and hippocampus tissue of newborn rats with hypoxic-ischemic encephalopathy(HIE).Methods Thirty 7-day-old neonatal rats were randomly divided into 3 groups:sham-operated group,hypoxic-ischemic(HI) group and pretreatment group.Rats in HI group and pretreatment group were subjected to left common carotid artery ligation,then were exposed to 80 mL/L oxygen and 920 mL/L nitrogen gas in 37 ℃ closed container for up to 2.5 h to establish HIE model.Progesterone was injected intraperitoneally into rats in the pretreatment group respectively for 30 minutes before hypoxia,and solution was injected into the sham-operated group and HI group.All rats were killed at 24 h after operation.The neuron apoptosis was identified and analyzed by flow cytometry.Nitrate/nitrite was assayed to represent nitric oxide content of brain tissues.Results The ratio of neuronal apoptosis and NO contents in cortex and hippocampus tissue in HI group [(10.09?0.36)%,(12.32?0.28)%,(51.36?9.71) ?mol/L,(52.34?4.26) ?mol/L] were significantly higher than those in sham-operated group [(2.49?0.23)%,(2.58?0.26)%,(18.16?6.24) ?mol/L,(19.28?3.58) ?mol/L)](P_a

This paper studied the relationship between apolipoprotein E isoforms and hyperlipidemia among 92 cases of diabetes mellitus, 174 cases with impaired glucose tolerance and 124 sex-age-matched controls. The results demonstrated that the patients with abnormal glucose tolerance had higher frequency of E2/3 isoforms and lower frequency of E, / , in com parison with controls. Hyperlipoproteinemia were mainly related to hyperglycemia but the Apo E isoforms which ex pressed different alleles also associated with hyperlipoproteinemia.

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.