OBJECTIVE: To determine the expression of palate, lung, and nasal epithelial clone (PLUNC) in na sal polyps (NP) and evaluate its association with clinical severity. METHOD: Twenty-eight NP patients (primary polyp, 15; recurrent polyp, 13) and 16 normal controls (healthy uncinate process) were enrolled, the expression of PLUNC was examined in nasal tissues by immunohistochemistric staining, quantitative PCR and ELISA respectively. The protein level of PLUNC in nasal polyps was correlated with nasal symptom score (nasal congestion and rhinorrhea, respectively). RESULT: PLUNC was mainly distributed in the epithelial layer and submucosal glands in nasal tissues. The staining intensity and mRNA level of PLUNC were significantly decreased in polyp tissues than in normal controls (P < 0.01). The protein levels of PLUNC were 0.33 +/- 0.11 and 0.15 +/- 0.05 in primary and recurrent polyp tissues (P < 0.01), and were 0.32 +/- 0.14 and 0.19 +/- 0.07 in small-size and big-size polyp tissues (P < 0.05). The protein level of PLUNC in polyp tissues significantly correlated with both nasal congestion score and rhinorrhea score (r = -0.51 and r = -0.57, P < 0. 01). CONCLUSION Decreased PLUNC in polyp tissues indicated that impaired innate immunity may account for the pathogenic process of NP. Thus upregulating PLUNC may represent a promising therapeutic target for the management of NP.
Adult ; Case-Control Studies ; Female ; Glycoproteins ; metabolism ; Humans ; Male ; Middle Aged ; Nasal Polyps ; metabolism ; pathology ; surgery ; Phosphoproteins ; metabolism ; Recurrence ; Young Adult

Objective To explore the relationship of serum levels of β-amyloid precursor protein (β-APP) with degree of traumatic brain injury (TBI) and the traumatic time.Methods Sprague-Dawley (SD) rats were randomly divided into normal control and injury group.The rats in injury groups suffered from TBI after free-falling percussion with different pressure (wild-injury,moderate-injury and severe-injury group).Then serum was collected at 0.5 h,2 h,6 h,and 24 h and subject to β-APP detection by ELISA.All data were analyzed statistically with completely randomized design multiple factor repeated measure of variance analysis and least significant difference (LSD) test.Results The serum levels of β-APP were higher after injury.The serum levels of β-APP were significantly higher in moderate-injury or severe-injury group than those in normal group or slight-injury group (P＜0.05).The serum levels of β-APP were higher in severe-injury group than that in moderate-injury group with no statistical difference (P＞0.05).There was no statistical difference in serum β-APP levels between normal control and slight-injury group (P＞0.05).Conclusion The serum level of P-APP is increasingly higher with traumatic brain injury more serious and could be employed as an indicator of TBI degree.It implies that β-APP has the potential as an early diagnosis marker for TBI.

OBJECTIVETo explore the role of ZNF217 in regulating cell proliferation, migration and invasion in glioma cells.

METHDOSA lentivirus-mediated shRNA-ZNF217 vector was infected into glioma U251 cells, and the interference efficiency was examined by Western blotting. MTT assay, flow cytometry, Transwell assay, and Boyden chamber assay were used to analyze the changes in cell proliferation, migration and invasion. Western blotting was used to detect the changes in ZNF217-related genes in the cells.

RESULTSshRNA-ZNF217 transfection significantly inhibited the expression of ZNF217 in U251 cells and suppressed the cell migration, invasion, growth, and cell cycle transition. ZNF217 knockdown downregulated the expression of pPI3, pAKT, C-Myc, and the mesenchyme biomarker N-cadherin, and stimulated the expression of the epithelium biomarker E-cadherin.

CONCLUSIONZNF217 promotes cell migration, invasion, and growth by activating PI3K/AKT signal to upregulate C-Myc and by modulating the genes associated with epithelial-mesenchymal transition in glioma cells.

Cadherins ; metabolism ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Epithelial-Mesenchymal Transition ; Genetic Vectors ; Glioma ; pathology ; Humans ; Lentivirus ; Neoplasm Invasiveness ; RNA, Messenger ; RNA, Small Interfering ; genetics ; Trans-Activators ; genetics ; Transfection

Objective To study the effect of β-aescine sodium on tumor necrosis factor α (TNF-α) in patient with severe traumatic brain injury and the clinical significance. Methods 60 patients with severe traumatic brain injury were divided equally into control group (n=30) and treatment group (n=30), who accepted routine therapy and further β-aescine sodium respectively. The serum TNF-α was determined before and 1 d, 2 d, 3 d, 5 d and 7 d after treatment. The patients were assessed with Glasgow Outcome Scale (GOS) 3 months after treatment.Results There was significant difference of serum TNF-α between treatment group and control group since 3 d after treatment (P<0.05). The score of GOS was better in the treatment group than in the control group 3 months after treatment (P<0.05). Conclusion β-aescine sodium is effective on severe traumatic brain injury. Level of TNF-α may be related with the outcome of patients with severe traumatic brain injury.

OBJECTIVE: To investigate the effect of curcumin on the invasion and migration of human glioma cells and explore the molecular mechanisms. METHODS: MTT assay was used for screening the optimal curcumin concentrations. The effects of curcumin on the invasion and metastasis of human glioma cell lines U251 and LN229 were tested using Transwell assay, Boyden assay and wound-healing assays. The expression of the related proteins and their interactions were determined using Western blotting and coimmunoprecipitation assay. RESULTS: Curcumin at the concentration of 20 μmol/L for 48 h was used as the optimal condition for subsequent cell treatment. In the two glioma cell lines, curcumin significantly suppressed the invasion and migration of the cells ( < 0.05) and lowered the expressions of hepatoma-derived growth factor (HDGF), Ncadherin, vimentin, Snail and Slug, but increased the expression of E-cadherin. Interference of HDGF in curcumin-treated glioma cells synergistically inhibited the epithelial-mesenchymal transition (EMT) signals, while overexpression of HDGF significantly reversed the inhibitory effect of curcumin on EMT; curcumin treatment could significantly reduce the binding of HDGF to β-catenin. CONCLUSIONS Curcumin suppresses EMT signal by reducing HDGF/β-catenin complex and thereby lowers the migration and invasion abilities of human glioma cells .
Cell Line, Tumor ; Cell Movement ; Curcumin ; Epithelial-Mesenchymal Transition ; Glioma ; Humans ; Intercellular Signaling Peptides and Proteins ; Neoplasm Invasiveness ; beta Catenin