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.

Objective To investigate the application effect of centralized health education among low-income parents in neonatal intensive care unit ( NICU) . Methods A total of 200 cases, who had low income parents and admitted to NICU from December 2012 to June 2013, were randomly divided into observation group (100 cases) and control group (100 cases). The neonatus in the control group underwent conventional health education mode, while neonatus in the observation group received conventional health education model based on a new type of health education on adoption. The awareness of health education, medical compliance and satisfaction of nursing assessed by self-designed health education effect scale, self-realization medical compliance and the satisfaction questionnaire in our hospital for quality of care. Results The satisfaction for quality of care in the experimental group was 97. 0% higher than 84. 0% in the control group (χ2 =9. 83,P<0. 01). The knowledge control of parents after health education in the experimental group was better than that in the control group (P<0. 01). Similarly, the medical compliance of neonatal parents in the experimental group was better than that of control group including treatment (92. 0%), treatment cooperation (95. 0%), payment on time (100. 0%) and visit as required (90.%) (χ2 =20. 37,20. 41,18. 58,14. 59, respectively;P <0. 01). Conclusions The centralized health education can facilitate the knowledge control of low-income parents in NICU, satisfaction of health education and medical compliance, and is worth of clinical promotion.

Objective:To investigate the inhibitory effect of ferulic acid on the retina of diabetic mice and high glucose-induced human retinal pigment epithelium (RPE) cell injury and the mechanism.Methods:Thirty 8-week-old SPF male type 2 diabetic db/db mice were selected and divided into a model group and a ferulic acid group by the random number table method, with 15 mice in each group.Another 15 db/m mice of the same age were selected as a control group.The model and control groups received normal saline (5 ml/kg) by gavage daily, and the ferulic acid group received ferulic acid solution (0.05 g/kg) by gavage daily.After two months of treatment, the mice were sacrificed and the eyeballs were removed.The morphological changes of mouse retinal tissues were observed by hematoxylin-eosin staining.The fluorescence intensity and expression levels of mitochondrial calcium uniporter (MCU), p38 mitogen-activated protein kinase (p38 MAPK) and phosphorylated p38 MAPK (p-p38 MAPK) in mouse retinal tissues were detected by immunofluorescence staining and Western blot.Human RPE cells were divided into control group, dimethyl sulfoxide (DMSO) group, high glucose group and high glucose+ ferulic acid group.The control group received no treatment, and the other cell groups were cultured with the corresponding reagents for 24 hours.The reactive oxygen (ROS) level of RPE cells in each group was detected with the ROS detection kit.The mitochondrial membrane potential level of RPE cells was detected with the a mitochondrial membrane potential detection kit (JC-1).The MCU and microfilament fluorescence intensity of RPE cells were detected with the a microfilament green fluorescent probe.To explore the regulatory relationship between MCU, p38 MAPK and p-p38 MAPK, the MCU protein level was silenced and overexpressed by lentivirus transfection technology.The fluorescence intensity and expression levels of MCU, p38 MAPK and p-p38 MAPK proteins in RPE cells were detected by immunofluorescence staining and Western blot.The use and feeding of experimental animals followed the 3R principle and the Statement of the Association for Research in Vision and Ophthalmology on the Use of Animals in Ophthalmology and Vision Research.This study protocol was approved by the Ethics Committee of Ningxia Eye Hospital, People's Hospital of Ningxia Hui Autonomous Region (No.2019085).Results:The intercellular space of the outer nuclear layer, inner nuclear layer and ganglion cell layer of the retinal tissue in the model group was increased and the cell arrangement was disordered compared with the control group, and the retinal tissue in the ferulic acid group was significantly improved.Compared with the control group, the fluorescence intensity of MCU, p-p38 MAPK and MCU+ p-p38 MAPK protein of mouse retinal tissue in model group and ferulic acid group was significantly increased (all at P<0.05).Compared with the model group, the fluorescence intensity of MCU, p-p38 MAPK and MCU+ p-p38 MAPK protein of mice retinal tissue in ferulic acid group was significantly decreased (all at P<0.05).Compared with the control group, the relative expression levels of MCU, p38 MAPK and p-p38 MAPK proteins of mouse retinal tissue in model group were significantly increased (all at P<0.05).Compared with the model group, the relative expression levels of MCU, p38 MAPK and p-p38 MAPK proteins of mice retinal tissue in ferulic acid group were significantly decreased (all at P<0.05).The ROS fluorescence intensities in the control group, DMSO group, high glucose group and high glucose+ ferulic acid group were 0.22±0.02, 0.22±0.03, 0.30±0.02 and 0.24±0.02, respectively, and the overall difference was statistically significant ( F=7.845, P<0.01).The ROS fluorescence intensity was significantly higher in the high glucose group than in the control and DMSO groups, and it was significantly lower in the high glucose+ ferulic acid group than in the high glucose group (all at P<0.05).The mitochondrial membrane potential was significantly lower in high glucose group and high glucose+ ferulic acid group than in control and DMSO groups, and significantly higher in high glucose+ ferulic acid group than in high glucose group (all at P<0.05).Compared with the control group and DMSO group, the fluorescence intensity of MCU was higher in the high glucose group, accompanied by the decrease and thinning of cell microfilaments, and the fluorescence intensity of MCU protein was significantly decreased in high glucose+ ferulic acid group, with the number of microfilaments increased significantly.Compared with the control group and DMSO group, the fluorescence intensity and relative expressions of MCU, p38 MAPK and p-p38 MAPK proteins were significantly increased in the high glucose group (all at P<0.05).Compared with the high glucose group, the fluorescence intensity and relative expressions of MCU, p38 MAPK and p-p38 MAPK proteins were significantly decreased in the high glucose+ ferulic acid group (all at P<0.05).Compared with the control group and the empty vector group, the relative expressions of MCU, p38 MAPK and p-p38 MAPK proteins were significantly increased in the MCU overexpression group and significantly decreased in the MCU shRNA group and the MCU overexpression+ ferulic acid group (all at P<0.05).Compared with MCU overexpression group, the relative expressions of MCU, p38 MAPK and p-p38 MAPK proteins were significantly decreased in MCU shRNA group and MCU overexpression+ ferulic acid group, and the differences were statistically significant (all at P<0.05). Conclusions:Ferulic acid can regulate oxidative stress and mitochondrial dysfunction, thereby ameliorating retinal damage and high glucose-induced RPE cell injury in diabetic mice, which may play a protective role through MCU and p38MAPK signaling pathways.