大規模トマト施設生産から排出されるトマト残渣量の推定とその堆肥化物の諸性質

It was estimated 11.6 kg・m^2 of leaves and 8.7kg・m^2 of fruits were released from the year-round tomato production at the rate of 40kg・m^2. Even though there will be some difference among the tomato varieties, one third of assimilate was discarded as the wastes by production, which was consisted of 60% of leaves and 40% of fruits. Compost of 0.75m^3 (308kg wet matter) was produced within this term (ten weeks), whose volume and weight were reduced by the half and 17% of initial amount, respectively. Temperature at the center of the secondary compost synchronized with air temperature with almost half-day delay, which meant the compost temperature was little increased by secondary fermentation. Inhibitory factor in germination have not been recognized on the every tested composts from tomato residues (tomato compost). Because tomato compost resembled to commercial bark compost in the water holding characteristics and mineral contents, the application of this compost was assumed as soil conditioner or medium for hydroponics. It is estimated that 49gN1・m^2 and 5.5kg CO_2・m^2 were released from tomato composting process on a year-round production. Simultaneously, 21g P・m^2 was also generated as am anure from this process

Enhanced Cytotoxic Effects of Arenite in Combination with Active Bufadienolide Compounds against Human Glioblastoma Cell Line U-87

The cytotoxicity of a trivalent arsenic derivative (arsenite, AsIII) combined with arenobufagin or gamabufotalin was evaluated in human U-87 glioblastoma cells. Synergistic cytotoxicity with upregulated intracellular arsenic levels was observed, when treated with AsIII combined with arenobufagin instead of gamabufotalin. Apoptosis and the activation of caspase-9/-8/-3 were induced by AsIII and further strengthened by arenobufagin. The magnitude of increase in the activities of caspase-9/-3 was much greater than that of caspase-8, suggesting that the intrinsic pathway played a much more important role in the apoptosis. An increase in the number of necrotic cells, enhanced LDH leakage, and intensified G2/M phase arrest were observed. A remarkable increase in the expression level of γH2AX, a DNA damage marker, was induced by AsIII+arenobufagin. Concomitantly, the activation of autophagy was observed, suggesting that autophagic cell death associated with DNA damage was partially attributed to the cytotoxicity of AsIII+arenobufagin. Suppression of Notch signaling was confirmed in the combined regimen-treated cells, suggesting that inactivation of Jagged1/Notch signaling would probably contribute to the synergistic cytotoxic effect of AsIII+arenobufagin. Given that both AsIII and arenobufagin are capable of penetrating into the blood–brain barrier, our findings may provide fundamental insight into the clinical application of the combined regimen for glioblastoma.p.21 Article number: 6577 Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)