• Journal of the Korea Organic Resources Recycling Association
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• v.20 no.2
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• pp.66-75
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• 2012

The objective of this study was to assess the effects of methanogenic bacteria-activated leachate recirculation method for enhancing waste stabilization and landfill gas production from a solid waste landfill. To simulate a conventional landfill (Lys-A), a landfill recirculated only fresh leachate (Lys-B), and two landfills recirculated leachate after pretreating with ASBR (Lys-C and Lys-D), four lysimeters were operated over a period of 4 years. Lys-D was recirculated two times of pretreated leachate volume than that of Lys-C. In the case of the landfill recirculated only fresh leachate and the landfill recirculated leachate after pretreating with ASBR, methane productions were increased until about 600 days, but there were not effect of leachate recirculation for enhancing methane production after about 600 days. It was assumed that leachate recirculation into fewer biodegradable organic wastes had not effect to enhance landfill gas production. Lys-C and Lys-D showed the highest performance for enhancing cumulative methane yield as well as acceleration waste stabilization. In cumulative methane yield, Lys-C (35.51 mL $CH_4/g$ VS) and Lys-D (36.12 mL $CH_4/g$ VS) were much higher than Lys-A (28.37 mL $CH_4/g$ VS) and Lys-B (30.07 mL $CH_4/g$ VS). In case of between Lys-B and Lys-C with the same recirculation rate, COD concentration in Lys-C was more rapidly decreased compared with that in Lys-B. This was attributed to the presence of methanogenic bacteria as well as dilution of inhibitory substances by the methanogenic bacteria-activated leachate recirculation. Therefore, the landfill recirculated leachate after pretreating with ASBR was found to be the most appropriate operating techniques for enhancing waste stabilization and landfill gas production.

• 한국유가공학회:학술대회논문집
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• 2007.09a
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• pp.49-58
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• 2007

Inflammatory process leads to the well-known mucosal damage and therefore a further disturbance of the epithelial barrier function, resulting abnormal intestinal wall function, even further accelerating the inflammatory process[1]. Despite of the records, etiology and pathogenesis of IBD remain rather unclear. There are many studies over the past couple of years have led to great advanced in understanding the inflammatory bowel disease(IBD) and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses including increased serum concentrations of different cytokines. Therefore, targeted molecules can be specifically eliminated in their expression directly on the transcriptional level. Interesting therapeutic trials are expected against adhesion molecules and pro-inflammatory cytokines such as TNF-${\alpha}$. The future development of immune therapies in IBD therefore holds great promises for better treatment modalities of IBD but will also open important new insights into a further understanding of inflammation pathophysiology. Treatment of cytokine inhibitors such as Immunex(Enbrel) and J&J/Centocor(Remicade) which are mouse-derived monoclonal antibodies have been shown in several studies to modulate the symptoms of patients, however, theses TNF inhibitors also have an adverse effect immune-related problems and also are costly and must be administered by injection. Because of the eventual development of unwanted side effects, these two products are used in only a select patient population. The present study was performed to elucidate the ability of TNF-${\alpha}$ antibodies produced in sheep colostrums to neutralize TNF-${\alpha}$ action in a cell-based bioassay and in a small animal model of intestinal inflammation. In vitro study, inhibitory effect of anti-TNF-${\alpha}$ antibody from the sheep was determined by cell bioassay. The antibody from the sheep at 1 in 10,000 dilution was able to completely inhibit TNF-${\alpha}$ activity in the cell bioassay. The antibodies from the same sheep, but different milkings, exhibited some variability in inhibition of TNF-${\alpha}$ activity, but were all greater than the control sample. In vivo study, the degree of inflammation was severe to experiment, despite of the initial pilot trial, main trial 1 was unable to figure out of any effect of antibody to reduce the impact of PAF and LPS. Main rat trial 2 resulted no significant symptoms like characteristic acute diarrhea and weight loss of colitis. This study suggested that colostrums from sheep immunized against TNF-${\alpha}$ significantly inhibited TNF-${\alpha}$ bioactivity in the cell based assay. And the higher than anticipated variability in the two animal models precluded assessment of the ability of antibody to prevent TNF-${\alpha}$ induced intestinal damage in the intact animal. Further study will require to find out an alternative animal model, which is more acceptable to test anti-TNF-${\alpha}$ IgA therapy for reducing the impact of inflammation on gut dysfunction. And subsequent pre-clinical and clinical testing also need generation of more antibody as current supplies are low.