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1‐Methylcyclopropene (1‐MCP) has been shown to be a suitable inhibitor of ethylene production in fruit and vegetables during preservation and distribution. In this study, a 1‐MCP controlled‐release system on coated paper was produced using shellac as the coating material. The effect of humidity and temperature on the release of 1‐MCP from the coated paper was investigated using a dynamic sorption system (DVS) with stepwise humidity changes (initial 20% relative humidity (RH) for 2 h, then increased to 40%, 50%, 60%, and 80% RH for 2 h, respectively). The release rate kinetic data were simulated using an Avrami equation with a mechanism release number n of 1.26. The results showed that the dynamic release of 1‐MCP from the coated paper was mainly affected by humidity, for which the release rate constant could be correlated with moisture concentration in humid air. The highest humidity condition (80% RH) resulted in the highest apparent activation energy of 46.8 kJ/mol. The effect of 1‐MCP coated paper on apple storage was evaluated by measuring the ethylene production rate, flesh firmness, and titratable acidity (TA) of apple. Ethylene production rates of apple were significantly affected with 1‐MCP coated paper. The values were 0.22 nL/g FW/h at 50 mg of 1‐MCP powder and 44.7 nL/g FW/h at 0 mg of 1‐MCP powder after 15 days at 4°C and 15 days at 20°C. The other properties of apple such as flesh firmness and TA also indicated that 1‐MCP coated paper could delay fruit softening during storage time. Based on these results, the release of 1‐MCP could be controlled by coating paper with shellac solution and promising to produce functional packaging for fruit. [ABSTRACT FROM AUTHOR]

ABSTRACT Serological surveys were performed on Ethiopian camels with a history of abortion to investigate the presence of antibodies against viruses that infect animals classified in the order Artiodactyla. In 2013, 120 serum samples were collected from camels in various parts of Ethiopia. Several viruses related to abortion in ruminants were prevalent. In particular, antibodies against bluetongue virus, were detected at a high rate (76.7% of samples). Additionally, antibodies against Akabane virus and Japanese encephalitis virus were also detected in samples from more than 40% of the camels; however, their antibody titers were relatively low. [ABSTRACT FROM AUTHOR]

Cyclooxygenase-2 (COX-2) plays an important role in tumorigenesis through prostaglandin E (PGE) biosynthesis. It has been shown by in vitro studies that PGE signaling transactivates epidermal growth factor receptor (EGFR) through an intracellular mechanism. However, the mechanisms underlying PGE-induced EGFR activation in in vivo tumors are still not fully understood. We previously constructed transgenic mice that develop gastric tumors caused by oncogenic activation and PGE pathway induction. Importantly, expression of EGFR ligands, epiregulin, amphiregulin, heparin-binding EGF-like growth factor, and betacellulin, as well as a disintegrin and metalloproteinases (ADAMs), ADAM8, ADAM9, ADAM10, and ADAM17 were significantly increased in the mouse gastric tumors in a PGE pathway-dependent manner. These ADAMs can activate EGFR by ectodomain shedding of EGFR ligands. Notably, the extensive induction of EGFR ligands and ADAMs was suppressed by inhibition of the PGE receptor EP4. Moreover, EP4 signaling induced expression of amphiregulin and epiregulin in activated macrophages, whereas EP4 pathway was required for basal expression of epiregulin in gastric epithelial cells. In contrast, ADAMs were not induced directly by PGE in these cells, suggesting indirect mechanism possibly through PGE-associated inflammatory responses. These results suggest that PGE signaling through EP4 activates EGFR in gastric tumors through global induction of EGFR ligands and ADAMs in several cell types either by direct or indirect mechanism. Importantly, gastric tumorigenesis of the transgenic mice was significantly suppressed by combination treatment with EGFR and COX-2 inhibitors. Therefore, it is possible that inhibition of both COX-2/PGE and EGFR pathways represents an effective strategy for preventing gastric cancer. ( Cancer Sci 2011; 102: 713-719) [ABSTRACT FROM AUTHOR]

The development of gastric cancer is closely associated with Helicobacter pylori ( H. pylori) infection. The expression of cylooxigenase-2 (COX-2), a rate-limiting enzyme for prostaglandin biosynthesis, is induced in H. pylori-associated chronic gastritis, which thus results in the induction of proinflammatory prostaglandin, PGE2. The COX-2/PGE2 pathway plays a key role in gastric tumorigenesis. On the other hand, several oncogenic pathways have been shown to trigger gastric tumorigenesis. The activation of Wnt/β-catenin signaling is found in 30–50% of gastric cancers, thus suggesting that Wnt signaling plays a causal role in gastric cancer development. Mutations in the bone morphogenetic protein (BMP) signaling pathway are responsible for the subset of juvenile polyposis syndrome (JPS) that develops hamartomas in the gastrointestinal tract. BMP suppression appears to contribute to gastric cancer development because gastric cancer risk is increased in JPS. Wnt signaling is important for the maintenance of gastrointestinal stem cells, while BMP promotes epithelial cell differentiation. Accordingly, it is possible that both Wnt activation and BMP suppression can cause gastric tumorigenesis through enhancement of the undifferentiated status of epithelial cells. Recent mouse model studies have indicated that induction of the PGE2 pathway is required for the development of both gastric adenocarcinoma and hamartoma in the Wnt-activated and BMP-suppressed gastric mucosa, respectively. This article reviews the involvement of the PGE2, Wnt, and BMP pathways in the development of gastric cancer, and gastric phenotypes that are found in transgenic mouse models of PGE2 induction, Wnt activation, BMP suppression, or a combination of these pathways. ( Cancer Sci 2009; 100: 1779–1785) [ABSTRACT FROM AUTHOR]

The activation of Wnt/β-catenin signalling has an important function in gastrointestinal tumorigenesis. It has been suggested that the promotion of Wnt/β-catenin activity beyond the threshold is important for carcinogenesis. We herein investigated the role of macrophages in the promotion of Wnt/β-catenin activity in gastric tumorigenesis. We found β-catenin nuclear accumulation in macrophage-infiltrated dysplastic mucosa of the K19-Wnt1 mouse stomach. Moreover, macrophage depletion in ApcΔ716 mice resulted in the suppression of intestinal tumorigenesis. These results suggested the role of macrophages in the activation of Wnt/β-catenin signalling, which thus leads to tumour development. Importantly, the conditioned medium of activated macrophages promoted Wnt/β-catenin signalling in gastric cancer cells, which was suppressed by the inhibition of tumour necrosis factor (TNF)-α. Furthermore, treatment with TNF-α induced glycogen synthase kinase 3β (GSK3β) phosphorylation, which resulted in the stabilization of β-catenin. We also found that Helicobacter infection in the K19-Wnt1 mouse stomach caused mucosal macrophage infiltration and nuclear β-catenin accumulation. These results suggest that macrophage-derived TNF-α promotes Wnt/β-catenin signalling through inhibition of GSK3β, which may contribute to tumour development in the gastric mucosa. [ABSTRACT FROM AUTHOR]