The widespread contamination of surface and ground water quality from the heavy use of fertilizer in modern agriculture is the current concern. Therefore, this study was carried out to develop a slow-release fertilizer using charcoal. The morphology of the charcoal impregnated fertilizer was investigated by scanning electron microscopy (SEM). This study also evaluated the release patterns of N, P, and K from impregnated charcoal using a simulated soil solution and distilled water as leaching solutions. The patterns of N, P, and K releases were examined in both static and continuous-flow conditions for 360 h. Releases of N, P, and K from impregnated charcoal were found to be slow and steady. However, the release trends of N, P, and K were higher in soil solution than distilled water under both the above conditions. Dissolution occurred when N, P, and K were released in the above leached solutions. As a result, the fertilizer impregnated charcoal could be developed as slow-release type fertilizer to minimize the contamination.

Chloride intracellular channel 1 (CLIC1) is a promising therapeutic target in cancer due to its intrinsic characteristics; it is overexpressed in specific tumor types and its localization changes from cytosolic to surface membrane depending on activities and cell cycle progression. Ca2+ and reactive oxygen species (ROS) are critical signaling molecules that modulate diverse cellular functions, including cell death. In this study, we investigated the function of CLIC1 in Ca2+ and ROS signaling in A549 human lung cancer cells. Depletion of CLIC1 via shRNAs in A549 cells increased DNA double-strand breaks both under control conditions and under treatment with the putative anticancer agent chelerythrine, accompanied by a concomitant increase in the p-JNK level. CLIC1 knockdown greatly increased basal ROS levels, an effect prevented by BAPTA-AM, an intracellular calcium chelator. Intracellular Ca2+ measurements clearly showed that CLIC1 knockdown significantly increased chelerythrine-induced Ca2+ signaling as well as the basal Ca2+ level in A549 cells compared to these levels in control cells. Suppression of extracellular Ca2+ restored the basal Ca2+ level in CLIC1-knockdown A549 cells relative to that in control cells, implying that CLIC1 regulates [Ca2+]i through Ca2+ entry across the plasma membrane. Consistent with this finding, the L-type Ca2+ channel (LTCC) blocker nifedipine reduced the basal Ca2+ level in CLIC1 knockdown cells to that in control cells. Taken together, our results demonstrate that CLIC1 knockdown induces an increase in the intracellular Ca2+ level via LTCC, which then triggers excessive ROS production and consequent JNK activation. Thus, CLIC1 is a key regulator of Ca2+ signaling in the control of cancer cell survival.

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To help address the physical, chemical, and biological degradation of agricultural soils resulting from indiscriminate use of chemical fertilizers, we developed a slow-release fertilizer from waste paper and urea. This approach has the advantage of a slow-release fertilizer in that it avoids surface runoff or leaching of nutrients, while providing an excellent medium for the recycling of waste paper. The successful impregnation of urea into waste paper was confi rmed by scanning electron microscopy. This study also evaluated the release patterns of N from impregnated waste paper using a simulated soil solution and distilled water as leaching solutions. The release patterns of N were examined in both static and continuous-fl ow conditions for 720 h. Release of N from impregnated waste paper was found to be slow and steady, although the release rate of N was lower in distilled water than soil solution under both conditions.