Objective: To explore the antagonism of selenium enriched Spirulina platensis(Se-SP) to hepatocirrhosis by enhancement of cell proliferation and selenoenzyme activity.Method: The male SD rat hepatocirrhosis model was induced by thioacetamide(TAA),and Se-SP was supplemented.Hepatic histological analysis was performed and relative content of collagen(RCC %) was estimated using IBAS 2000 system after Masson’s staining.Glutathione peroxidase(GSH-Px),thioredoxin reductases(TR) and malondialdehyde(MDA) in hepatocyte as well as hyaluronic acid(HA) in serum were determined.Expression index of proliferating cell nuclear antigen(PCNA) in hepatocytes was detected by immu-nohistochemistry,and the level of synthesis of DNA in regenerative hepatocytes was analyzed by radio-immunity for incorporation of 3H-TDR.Results: Hepatocirrhosis was induced by TAA at 9w of the expeiment,and the obvious antagonism of Se-SP to hepatocirrhosis was obsewed after Se-SP supplementa-tion.12.5% rats of Se-Sp group were completely recovered at 15w of the experiment(6w after withdrawal of TAA).GSH-Px and TR activity in hepatocytes as well as PCNA and 3H-TDR incorporation rate in hepatocytes were obviously enhanced(P

Objective To analyze the clinical features of infective endocarditis with positive antineutrophil cytoplasmic antibodies ,and compare with ANCA associated small vessel vasculitis(AASV). Methods Three IE patients with positive ANCA were analyzed, and 13 cases from literatures were reviewed. Results Sixteen patients had positive anti-PR3 ANCA, in which 2 cases had both positive (anti-PR3 and anti-MPO ANCA) ANCA. All patients had some clinical manifestations mimic AASV, including fever ( 13/16, 81% ), rash (8/16, 50% ), rapidly progressive glomerulonephritis (7/16, 44% ), splenomegaly (6/16, 38% ). Streptococcal species were identified in 12 patients, and cardiac valvular abnormalities were demonstrated in all patients. All patients except 2, who died of cerebral hemorrhage followed by cerebral infarction, recovered with antibiotic therapy. Conclusion Infective endocarditis sometimes can have the same clinical features as AASV, so physicians should carefully differentiate between them when dealing with patients with positive ANCA antibodies.

[Objective]To study the expression of Cad-Ⅱ gene in bone marrow mesenchymal stem cells(MSCs) transfected with Cad-ⅡcDNA after autografted into the bone defects. [Method]The experimental model of ilium segment defect was established in 20 Japanese white rabbits.The rabbit MSCs were isolated,cultured and expanded in vitro,and then the MSCs,transfected with Cad-Ⅱ and compounded with collagen sponge were autografted into the ilium segment defect.At 4 weeks of operation,the MSCs/ collagen sponge were excised,and the expression of Cad-Ⅱ was evaluated with RT-PCR and immunohistochemical methods.[Result]All of the bone defects treated with implants exhibited new bone formation at 4 weeks postoperatively.In the transfection group,Cad-Ⅱ gene mRNA expression was higher than that in the control group(P

Objective To explore the significance of LDH and ?2-m concentration in CSF in differentiating viral meningitis from purulent meningitis in pediartic patients.Methods Kinetic method was performed to detect the LDH concentration in CSF in 45 patients with purulent meningitis and 49 patients with viral meningitis and 22 healthy children of control group respectively.On the other hand,radioimmunoassay(RIA)was used to detect the concentration of ?2-m.Results The concentrations of LDH in CSF in purulent meningitis group(26.15?12.17)U/L were higher than that in viral meningitis group(8.76?4.94)U/L significantly(P

Metabolomics, the newest “omics”science after genomics, thranscriptomics and proteomics, is the study of simultaneous identification and quantification of products of the biochemical reaction within an or-ganism. It has been used in the study of papillary thyroid cancer. This review presents an introduction to the con-cept and research techniques of metabolomics and the progress of application in papillary thyroid cancer.

Objective To investigate the clinical significance of antiendothelial cell antibodies (AECA) in systemic vasculitis. Method With Human umbilical vein endothelial cell (HUVEC) as substrate cell, sera from 129 systemic vasculitis patients [including 59 Behcet′s disease(BD), 28 Takayasu arteritis (TA), 20 Wegener′s granulomatosis (WG), 8 polyarteritis nodosa (PAN), 9 microscopic polyangiitis (MPA), 5 Churg-Strauss syndrome (CSS)] were screened for the presence of AECA by ELISA. Sera from SLE, RA and healthy donors were examined as controls. The association of AECA to clinical disease activity was analyzed. Result The prevalence of AECA by HUVEC cell-ELISA was 59% in systemic vasculitis [48% in BD,79% in TA, 65% in WG, 63% in PAN, 44% in MPA, 80% in CSS], 46% in SLE, 4% in RA, and 2.4% in control group. Compared with patients with RA and control group, AECA were more frequently found in patients with systemic vasculitis and SLE (P

Objective In our previous work, the prevalence of anti-endothelial cell antibodies(AECA) in patients with systemic vasculitis and other autoimmune diseases was analyzed. AECA against a 47 000 endothelial cell antigen was found in patients of a variety of systemic vasculitis and systemic lupus erythematosus (SLE). It was suggested to be α-enolase by the combination of immunoblotting and proteomics methods. The aim of this work is to demonstrate that α-enolase is one of the targets of AECA, and to detect the prevalence of anti-α-enolase antibody in sera of patients with autoimmune disorders including systemic vasculitis. Methods The CDS of human Enol gene was amplified by polymerase chain reaction (PCR), with template of human placenta λzap express Cdna library. The product was then recombined with expression vector. After expression and purification from E.coli, the recombinant protein was analyzed by mass spee-trometry. The prevalence of anti-α-enolase antibody in patients with autoimmune disorders including systemic vasculitis was tested by Western blot and enzyme-linked immunosorbent assay (ELISA). Results The CDS of human Enol gene was subcloned to the expression vector. Recombinant human α-enolase was expressed and purified in E.coli. The recombinant protein was demonstrated to be his-tagged human a-enolase by mass spectrometry. Results of Dot-Blot revealed that the prevalence of anti-α-enolase antibody was 76.7% in systemic vasculitis [including 74.0% in Behcet's disease (BD), 81.5% in Takayasu artefitis (TA), 62.5% in Wegener's granulomatosus (WG), 92.3% in microscopic polyangitis (MPA) and 80.0% in Churg-Stranss syndrome (CSS)], 78.3% in SLE, 63.6% in Sjogren's syndrome (SS) and 78.9% in rheumatoid arthritis(RA). No positive signals were detected in sera of normal controls or patients with polymyositis/ dermatomyositis (PM/DM). There was no statistical significance among positive rates of anti-α-enolase antibody in systemic vasculitis, SLE, SS or RA patients. The prevalence of positive signals at the most extensive level (+++～++++) was 51.7% in patients with systemic vasculitis, 33.3% in SLE, 42.9% in SS and 20.0% in RA. There was statistical significant difference between RA and systemic vasculitis. Conclusion The identification of human α-enolase as one of the targets of AECA and its prevalence in a variety of autoimmune disorders will shed some light on the understanding of the pathogenesis of vascular injury in autoimmune diseases.

Objective To analyze the clinical features of patients with hemophagocytic syndrome (HPS) in autoimmune diseases (AID). Methods We collected the data of 11 patients with AID complicated with HPS in Peking Union Medical College Hospital from 2004 to 2009. The underlying diseases, clinical features, laboratory findings and treatment outcomes were retrospectively analyzed. Results Of the 11 patients,3 were male,8 were female. Mean age was (30. 7 ± 18. 3) years. The underlying diseases included Still disease ( n = 4 ), systemic lupus erythematosus ( n = 3 ), and rheumatoid arthritis, primary Sj(o)gren's syndrome, Wegener granulomatosis and Crohn disease in each one case. HPS was associated with the onset of AID ( n = 4), active infection alone ( n = 1 ) and both factors ( n = 6 ). HPS was clinically characterized by high fever ( 100% ), hepatosplenomegaly ( 72. 7% ) , lymphadenopathy ( 63.3% ) and central nervous system involvement (36. 3% ). 4 patients presented with disseminated intravascular coagulation(DIC) (36. 3% ). Laboratory data mainly manifested with cytopenia ( 100% ), liver dysfunction ( 100% ), hypofibrinogenemia ( 62. 5% ), hypertriglyceridemia ( 81.8% ), serum ferritin ＞ 500 μg/L (100%), low NK-cell activity(80% ) and hemophagocytosis in bone marrow( 100% ). Based on treating underlying infections and use of corticosteroids and immunosuppressive agents in combination with intravenous immunoglobulins(IVIG) therapy, 5 patients recovered , 6 patients died. The mortality rate was 54. 5%. DIC were associated with mortality ( r = 0. 69, P = 0. 019 ). Conclusion The episode of HPS always occurs simultaneously with multiple system involvement that was often difficult to distinguish from active AID. The present of DIC on HPS related with poor prognosis and high mortality. Corticosteroids and immunodepressant and IVIG may improve the prognosis of HPS, while anti-infection therapy is very important and necessary for the patients accompany with active infection.

Objective To study the effect of Src tyrosine kinase inhibition on subcutaneously transplanted tumor of human lung adenocarcinoma in mice and its mechanism. Methods For the subcutaneously transplanted tumor model, A549 cells or PC-9 cells were inoculated into SCID mice by subcutaneous injection. Immunohistochemistry was used to show the effect of Src tyrosine kinase inhibition on proliferation index (Ki-67 staining) and microvessel density (CD31 staining) of subcutaneously transplanted tumor of human lung adenocarcinoma in mice. Results Subcutaneously transplanted tumor of PC-9 cells was sensitive to src tyrosine kinase inhibitor. There was significant difference between treatment group and control group (P <0.01). There was significant difference between the two treatment group too (P <0.01). Stopping treatment for 1 week, the inhibition rate of tumor growth were 33.19 % and 84.79 % in 10 mg·kg-1·d-1 and 50 mg·kg-1·d-1 treatment group, respectively. The same treatment was less effective to subcutaneous tumors produced by A549 cells. Treatment with 50 mg·kg-1·d-1 Src tyrosine kinase inhibitor significantly reduced the proliferation index of subcutaneously transplanted tumor produced by PC-9 cells (P<0.01) and tended to reduce the proliferation index of subcutaneously transplanted tumor produced by A549 cells (P >0.05). Treatment with 50 mg·kg-1·d-1 Src tyrosine kinase inhibitor significantly reduced micro vascular density in both PC-9 and A549 induced subcutaneous tumors (P <0.05). Conclusion Inhibition of Src tyrosine kinase could suppress the progression of subcutaneously transplanted tumor, not only by the inhibition of cell proliferation of lung adenocarcinoma cells directly, but also by the inhibition of angiogenesis indirectly.

Objective To investigate the role of soluble cytotoxic T-lymphocyte associated antigen-4 (sCTLA-4) in the pathogenesis of myasthenia gravis (MG) in Fujian province.Methods A total of 80 patients with MG and 80 sex-and age-matched healthy controls were enrolled in the study .MG patients were divided into non-glucocorticoid treatment group and glucocorticoid treatment group , and the latter was further divided into immunosuppressive therapy group and thymusectomy group .Concentrations of sCTLA-4 in ser-ums from above mentioned groups were measured by enzyme-linked immunosorbent assay (ELISA).Results The concentrations of sCTLA-4 in both non-glucocorticoid treatment group and glucocorticoid treatment group were significantly higher than those in the healthy control group (6.03 ng/ml±3.58 ng/ml, 3.44 ng/ml± 2.36 ng/ml vs.0.49 ng/ml±0.95 ng/ml) (χ2=100.67, P<0.001), but sCTLA-4 concentrations in glu-cocorticoid treatment group were lower than those in non-glucocorticoid treatment group (Z=-3.37,P=0.001).With the treatment of glucocorticoid, the sCTLA-4 concentrations were reduced (6.03 ng/ml± 3.58 ng/ml vs.4.56 ng/ml±2.08 ng/ml;t=3.10, P=0.005), and the concentrations of sCTLA-4 were also decreased after thymusectomy therapy (3.86 ng/ml±2.53 ng/ml vs.2.59 ng/ml±2.37 ng/ml; Z=-2.21, P=0.04).However, there was no significant difference in the concentrations of sCTLA-4 before and after immunosuppressive drugs treatment (Z=-1.26,P=0.21).Conclusion The concentration of sCTLA-4 was increased in patients with MG , but with the treatment of glucocorticoid or thymusectomy it could be reduced .