Objective To evaluate the clinical value of detecting serum underglycosylated IgA1 in diagnosis and differentiation of lgA nephropathy (IgAN). Methods Serum underglycosylated IgA1 was isolated by microspincolumn coupled with vicia villosa lectin (VVL) from 48 cases with IgAN and 43 cases with other primary glomemlonephritis. All the patients were diagnosed by renal biopsy. Sera from 20 healthy persons were used as control group. After isolation, the eluant with rich underglycosylated lgAl was detected by incubation with biotin- labeled horseradish peroxidase (HRP) and Helix aspersa (HAA, recognizing N-acetylgalactosamine specifically)in enzyme-linked immunosorbent assay (ELISA). The sensitivity and specificity of diagnosis and differentiation of IgAN with elevated serum underglycosylated IgA1 were analyzed. Results The level of serum underglycosylated IgA1 in IgAN patients [(83.7±41.0) U] was significantly higher than that in healthy control group [(52.6±22.9) U] and the patients with other primary glomerular diseases[(49.2±27.3) U] (all P<0.01). Twenty-two cases of non-IgA mesangial proliferative glomerulonephritis accounted for 51% of other primary glomerular disease, whose underglycosylated IgA1 level [(47.6±21.5 ) U] (all P<0.01 ) was significantly lower as compared to IgAN patients. Taking the renal biopsy diagnosis as golden diagnostic criteria, the ROC curve was performed. The area under the curve was 0.797 with a standard error 0.047 (P<0.01). The sensitivity as a diagnostic test was 72.9%, with specificity 72.1% and accuracy 72.5%. Conclusion Detection of serum underglycosylated lgAl level by mierospineolumn method and ELISA assay has certain clinical value in diagnosis and differentiation of IgAN.

Aim To observe the adhesive process of the human gastric cancer cell line MKN1,and study the expression of integrin ?1;to investigate the mechanism of the inhibition of the adhesion process of MKN1 cells by destran sulfate(DS).Methods The MKN1 cells were cultured with DS or PBS,then stained with immunofluorescent cytochemistry and observed in fixed or living conditions with confocal laser scanning microscope.RT-PCR was used to analyze the cDNA expression of MKN1 cells.Results MKN1 cells adhered to culture dishes by the process of forming filopodia,changed into a flat shape,and then adhered to other cells to form a cell-monolayer.Integrin ?1 was intensively expressed in the cell membrane,where integrin ?1 formed clusters.DS inhibted the expression of integrin ?1 in cell membrane,and decreased the area of integrin ?1 clusters.DS-treated cells also tended to maintain a round shape by contracting the filopodia.In DS-containing culture dishes,some cells kept floating 4 hours after seeding.DS decreased the level of the cDNA expression of the adhered cells to 74% and of the floating cells to 38% of that of the cells in un-treated group,respectively.Conclusion The inhibition of the adhesion of MKN1 cells by DS was related to the suppression of the expression of integrin ?1.

Objective To investigate the effect of IFN-γ on the proliferation and migration of esophageal squamous cell carcinoma cell line Eca9706 and related mechanism. Methods Cells were cultured in vitro and treated with interferon-γ. Cell morphology changes were observed under microscope, cell proliferation ability was detected by CCK-8 experiment, and cell migration ability was detected by cell scratch experiment and Transwell experiment. Real-time PCR method was used to detect the expression efficiency of chemokine CXCL8 (interleukin 8), and the ELISA experiment was used to detect the change of CXCL8 secretion. Results Compared with the blank control group, Eca9706 cells treated with different concentrations of interferon-γ did not change significantly in cell morphology. CCK8 experiment confirmed that the proliferation ability of Eca9706 cells after IFN-γ treatment was significantly reduced (P < 0.01). Cell scratch experiment found that IFN-γ significantly decreased the migration ability of Eca9706 cells (P < 0.01). Transwell experiment showed that after IFN-γ treatment, the migration ability of Eca9706 cells was significantly inhibited (P < 0.01). CXCL8 gene expression level in Eca9706 cells treated with interferon-γ was significantly down-regulated (P < 0.01), and the amount of CXCL8 secretion significantly reduced (P < 0.05). Conclusion Interferon-γ can inhibit the proliferation and migration of esophageal cancer cell line Eca9706, which may be related to its inhibition of the expression and secretion of CXCL8.