The effect of cognition need on information seeking behaviors of information users and the difference in behaviors of information users were investigated in 184 undergraduates from the same grade with different back-grounds of subjects using the cognition need scale and undergraduates information-seeking behaviors scale ,respec-tively.The data were analyzed by descriptive statistical analysis, correlation analysis, rank test, and multivariate linear regression analysis , respectively , showing that the cognition need is significantly correlated with the informa-tion seeking behaviors of undergraduates in terms of information evaluation, information searching, information management and information use .

OBJECTIVE: To study anti-inflammatory effect and mechanism of the luteolin · 4, 4' -dipyridy co-crystal.METHODS: Using macrophage RAW264. 7 of normal mice as control, the inflammation model was established with lipopolysaccharide (LPS) -induced RAW264. 7 cells. MTT assay was used to detect cells activity 2 h after treatment of different concentrations of luteolin (10, 20, 40, 80 μmol/L), 4, 4' -dipyridy (10,20, 40,80 μmol/L) and luteolin·4, 4' -dipyridy co-crystal (10, 20, 40, 80 μmol/L). The mRNA expression of iNOS and COX-2 in RAW264. 7 cells at 40 μmol/L were determined by qRT-PCR. The protein expression of TNF-α and IL-6 in RAW264. 7 cells at 40 μmol/L were determined by ELISA. The protein expression of NF-κB p65 in RAW264. 7 cells at 40 μmol/L were determined by Western bolt. RESULTS: Compared with normal cells, the activity of RAW264. 7 cells was decreased significantly after induced by LPS (P<0. 01); mRNA expression of iNOS and COX-2, protein expression of TNF-α, IL-6 and NF-κB p65 were increased significantly (P<0. 01). Both luteolin and luteolin · 4, 4' -dipyridy co-crystal could enhance the activity of RAW264. 7 cells after induced by LPS (P<0. 05 or P<0. 01) in concentration-dependent manner. 4, 4' -dipyridy had no significant effect on the activity of RAW264. 7 cells after induced by LPS. After luteolin and luteolin· 4, 4' -dipyridy co-crystal at 40 μmol/L, mRNA expression of iNOS and COX-2, protein expression of TNF-α, IL-6 and NF-κB p65 in RAW264. 7 cells after induced by LPS were decreased significantly (P<0. 05 or P<0. 01); the luteolin · 4, 4' -dipyridy co-crystal was better than luteolin (P<0. 05 or P<0. 01). CONCLUSIONS: The luteolin·4, 4' -dipyridy co-crystal can inhibit the generation of inflammatory factors by down-regulating NF-κB signal, and its anti-i nflammatory effect is better than luteolin.

Gap junctions mediate direct communication between cells; however, toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Although cadmium (Cd) is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A rat liver cells has yet to be established. In this study, we showed that Cd treatment decreased the cell index (a measure of cellular electrical impedance) in BRL 3A cells. Mechanistically, we found that Cd exposure decreased expression of connexin 43 (Cx43), increased expression of p-Cx43 and elevated intracellular free Ca2+ concentration, corresponding to a decrease in gap junctional intercellular communication. Gap junction blockage pretreatment with 18β-glycyrrhizic acid (GA) promoted Cd-induced apoptosis, involving changes in expression of Bax, Bcl-2, caspase-3 and the mitochondrial transmembrane electrical potential (Δψm). Additionally, GA was found to enhance ERK and p38 activation during Cd-induced activation of mitogen-activated protein kinases, but had no significant effect on JNK activation. Our results indicated the apoptosis-related proteins and the ERK and p38 signaling pathways may participate in gap junction blockage promoting Cd-induced apoptosis in BRL 3A cells.
Animals ; Apoptosis/*drug effects ; Cadmium/*toxicity ; Calcium/metabolism ; Cell Communication/drug effects ; Connexin 43/genetics ; Enzyme Activation/drug effects ; Gap Junctions/*drug effects ; Gene Expression Regulation/drug effects ; Hepatocytes/cytology/*drug effects ; Rats ; Signal Transduction/drug effects

Objective:To evaluate the role of epidermal growth factor (EGF) in repair of lung tissues in mice with acute respiratory distress syndrome (ARDS).Methods:Fifty SPF male C57BL/6 mice, aged 6-8 weeks, weighing 21-23 g, were divided into 5 groups ( n=10 each) using a random number table method: control group (group C), EGF group, LPS+ PBS group, LPS+ EGF group and AG1478+ LPS+ EGF group.PBS 0.1 ml was intraperitoneally injected in group C. EGF 10 μg (0.1 ml) was intraperitoneally injected in group EGF.The equal volume of PBS and EGF 10 μg was intraperitoneally injected at 12 h after tracheal infusion of LPS in group LPS+ PBS and group LPS+ EGF, respectively.EGF receptor (EGFR) antagonist AG1478 1 mg was intraperitoneally injected, 30 min later LPS was tracheally instilled, and 12 h later EGF 10 μg was intraperitoneally injected in group AG1478+ LPS+ EGF.ARDS model was developed by endotracheal instillation of LPS 3 mg/kg.The mice were sacrificed on the 1st and 5th days after development of the model, and lung tissues were obtained for microscopic examination of the pathological changes which were scored after HE staining.Bronchoalveolar lavage was performed on 5th day after development of the model and before sacrifice, and bronchoalveolar lavage fluid (BALF) was collected to detect total protein concentration (by BCA method) and IL-6 and TNF-α concentrations (by enzyme-linked immunosorbent assay). Lung tissues were obtained for determination of the wet/dry lung weight ratio (W/D ratio), expression of lung surfactant associated protein C (SP-C) and proliferating nuclear antigen (PCNA) (by immunofluorescence method), and expression of EGFR, phosphorylated EGFR (p-EGFR), protein kinase B (Akt), and phosphorylated Akt (p-Akt) (by Western blot). Results:Compared with group C, the pathological score, W/D ratio, concentrations of total protein, IL-6 and TNF-α in BALF and neutrophil count were significantly increased, the number of cells co-expressing SP-C and PCNA was increased, and p-EGFR/EGFR and p-Akt/Akt ratios were increased in group LPS+ PBS ( P<0.01), and no significant change was found in the indexes mentioned above in group EGF ( P>0.05). Compared with group LPS+ PBS, the pathological score, W/D ratio, concentrations of total protein, IL-6 and TNF-α in BALF and neutrophil count were significantly decreased, the number of cells co-expressing SP-C and PCNA was increased, and p-EGFR/EGFR and p-Akt/Akt ratios were increased in group LPS+ EGF ( P<0.01). Compared with group LPS+ EGF, the pathological score, W/D ratio, concentrations of total protein, IL-6 and TNF-α in BALF and neutrophil count were significantly increased, the number of cells co-expressing SP-C and PCNA was decreased, and p-EGFR/EGFR and p-Akt/Akt ratios were decreased in group AG1478+ LPS+ EGF ( P<0.01). Conclusions:EGF can promote the repair of lung tissues in mice with ARDS, and the mechanism may be related to activation of EGFR signaling pathway and promotion of proliferation of alveolar epithelial cell type Ⅱ.