Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.

Epidermal growth factor (EGF) has been shown to induce intestinal proliferation and maturation; however, little information is available regarding substrates of the intestinal EGF receptor tyrosine kinase. The purpose of this study was to determine if src homologous collagen-like protein (Shc) was an in vivo substrate of the intestinal EGF receptor.', 'Ten-day-old rats were treated with EGF or were breast-fed. In some experiments, IEC-6 cells were treated with EGF. Intestinal tissue and cell fractions were studied by immunodetection to compare the tyrosine phosphorylation state and the subcellular localization of intestinal proteins.', 'The total tyrosine phosphorylation state of intestinal proteins was increased threefold by EGF. Tyrosine phosphorylation of the EGF receptor and Shc were rapidly increased by EGF. The association of Grb2 with Shc increased fourfold and fivefold. Plasma membrane translocation of Shc and associated phosphotyrosyl proteins was increased within 30 seconds of EGF treatment.
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Disseminated intravascular coagulation (DIC) is a complex systemic thrombohemorrhagic disorder involving intravascular coagulation and hemorrhage. The aim of this study is to test whether static magnetic field (SMF) is effective in attenuating lipopolysaccharide (LPS)-induced DIC.', 'In vivo experiments were performed in this study using male BALB/cByJ mice. An intraperitoneal injection of 50 mg/kg LPS was shown to lead to approximately 50% mortality and this dose was used in subsequent experiments. To test the effects of SMF on the survival rate of LPS-induced animals, the mice were exposed to 0.25-T SMF for 2 h before LPS injection. In addition, the effect of a 2-h SMF treatment on the production of anti-inflammatory cytokines was evaluated.', 'In the first set of experiments, we found that the survival rate was higher in the SMF-exposed group than in the sham-exposed group. The circulating platelet (PLT) counts in the SMF-exposed mice were significantly higher than in the unexposed animals. However, no significant changes in inflammatory cytokine, including tumour necrosis factor-alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1), in plasma were found after SMF treatment. The results from the second experiment showed that the plasma levels of interleukin-1 receptor antagonist (IL-1ra) were higher in the SMF-exposed group than in the sham group.
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Oral epithelial cells have currently been found to play an important role in inflammatory modulation in periodontitis. Mangiferin is a natural glucosylxanthone with anti-inflammatory activity. The aim of this study was to investigate the regulatory effect of mangiferin on lipopolysaccharide (LPS)-induced production of proinflammatory cytokine interleukin-6 (IL-6) in oral epithelial cells and the underlying mechanisms.', 'The levels of LPS-induced IL-6 production in OKF6/TERT-2 oral keratinocytes were detected using enzyme-linked immunosorbent assay (ELISA). The expression of Toll-like receptor (TLR) 2 and TLR4 was determined using western blot analysis. And the phosphorylation of TLR downstream nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK) was examined using cell-based protein phosphorylation ELISA kits.', 'We found that mangiferin reduced LPS-upregulated IL-6 production in OKF6/TERT-2 cells. Additionally, mangiferin inhibited LPS-induced TLR2 and TLR4 overexpression, and suppressed the phosphorylation of NF-κB, p38 MAPK and JNK. Moreover, mangiferin repressed IL-6 production and TLR signaling activation in a dose-dependent manner after 24h treatment.

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