In May 2010, Indonesia and Norway signed a Letter of Intent on "Cooperation on Reducing Greenhouse Gas Emissions from Deforestation and Forest Degradation(REDD)." In the LoI, Norway agreed to offer Indonesia a sum of USD 1 billion with a view to encourage Indonesia to significantly contribute to the successful implementation of REDD+. On 20 May 2011, correspondingly, Indonesia announced the 2011 'Forest Moratorium' (the Presidential Instruction No. 10/2011) which was valid for the following consecutive two years. By means of the 2011 'Forest Moratorium', Indonesia aimed at significant reductions in greenhouse gas emissions from deforestation, forest degradation and peatland conversion. In so doing, it also sought to improve forest governance. Meanwhile, concerned stakeholders also raised various questions about the effectiveness of the 'Forest Moratorium'. As an extension of the 2011 'Forest Moratorium', Indonesia announced the 2013 'Forest Moratorium'(the Presidential Instruction No. 6/2013) for another two-year period on 13 May 2013. Indonesia's 'Forest Moratorium' is concerned with stakeholders at various levels, who may play a role of significant 'agent' in the process of implementing the 'Forest Moratorium'. This mechanism of the 'Forest Moratorium' should be understood in the light of forest governance. Employing stakeholder approach, therefore, this article attempts to analyze Indonesia's 'Forest Moratorium' in the light of forest governance. In this regard, it analyzes the detailed contents of the 'Forest Moratorium', the process of making the 'Forest Moratorium', current development of the Indicative Moratorium Map for suspension of new concessions on forest land, and contesting views of various stakeholders. At the same time, it also talks about how 'weak' forest governance had influence upon Indonesia's 'Forest Moratorium'. In so doing, this article consequently attempts to evaluate Indonesia's 'Forest Moratorium' and also put it into perspective in terms of improving forest governance. The 2013 'Forest Moratorium' fundamentally represents a radical policy that is designed to suspend new concessions on forest conversion for another two-year period and its detailed contents attempt to reflect on various stakeholders from related industries and environmental NGOs. However, there are challenging factors in the process of implementing the 'Forest Moratorium', that is, 'weak' forest governance and also a discrepancy between forest planning maps designated by central and regional governments. The announcement of the 2013 'Forest Moratorium', as an extension of the 2011 'Forest Moratorium', may functionally strengthen and improve Indonesia's forest governance. However, at the same time, there is a practical limit due to the fact that it is merely a Presidential Instruction that lacks legal binding.
The inhibitory effects of 5,6,3',5'-tetramethoxy 7,4'-hydroxyflavone (labeled as p7F) were elucidated on the productions of proinflammatory cytokines as well as inflammatory mediators in human synovial fibroblasts and macrophage cells. p7F inhibited IL-1${\beta}$ or TNF-${\alpha}$ induced expressions of inflammatory mediators (ICAM-1, COX-2, and iNOS). p7F also inhibited LPS-induced productions of nitric oxide and prostaglandin $E_2$ in RAW 264.7 cells. In order to investigate whether p7F would inhibit IL-1 signaling, p7F was added to the D10S Th2 cell line (which is responsive to only IL-1${\beta}$ and thus proliferates), revealing that p7F inhibited IL-1${\beta}$-induced proliferation of D10S Th2 cells in a dose-response manner. A flow cytometric analysis revealed that p7F reduced the intracellular level of free radical oxygen species in RAW 264.7 cells treated with hydrogen peroxide. p7F inhibited IkB degradation and NF-${\kappa}$B activation in macrophage cells treated with LPS, supporting that p7F could inhibit signaling mediated via toll-like receptor. Taken together, p7F has inhibitory effects on LPS-induced productions of inflammatory mediators on human synovial fibroblasts and macrophage cells and thus has the potential to be an anti-inflammatory agent for inhibiting inflammatory responses.
The tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is considered a promising anticancer agent due to its unique ability to induce cancer cell death having only negligible effects on normal cells. However, many cancer cells tend to be resistant to TRAIL. In this study, we investigated the effects and molecular mechanisms of sodium butyrate (SB), a histone deacetylase inhibitor, in sensitizing TRAIL-induced apoptosis in 5637 human bladder cancer cells. Our results indicated that co-treatment with SB and TRAIL significantly increased the apoptosis induction, compared with treatment with either agent alone. Co-treatment with SB and TRAIL effectively increased the cell-surface expression of death receptor (DR) 5, but not DR4, which was associated with the inhibition of cellular Fas-associated death domain (FADD)-like interleukin-1β-converting enzyme (FLICE) inhibitory protein (c-FLIP). Furthermore, the activation of caspases (caspase-3, -8 and -9) and degradation of poly(ADP-ribose) were markedly increased in 5637 cells co-treated with SB and TRAIL; however, the synergistic effect was perfectly attenuated by caspase inhibitors. We also found that combined treatment with SB and TRAIL effectively induced the expression of pro-apoptotic Bax, cytosolic cytochrome c and cleave Bid to truncated Bid (tBid), along with down-regulation of anti-apoptotic Bcl-xL expression. These results collectively suggest that a combined regimen of SB plus TRAIL may offer an effective therapeutic strategy for safely and selectively treating TRAIL-resistant bladder cancer cells.
Cervical cancer is one of the leading causes of female death from cancer worldwide with about 500,000 deaths per year. A strong association between certain human papilloma viruses (HPV type 16 and 18) and cervical cancer has been well known. An extract of Saururus chinensis, named as PE-46, has been used to investigate whether this agent has the ability of inhibiting the oncogenes E6 and E7 of HPV type 16. PE-46 inhibited the proliferation of human cervical cancer cell lines in a dose response manner. PE-46 also inhibited the in vitro binding of E6 and E6AP which are essential for the binding and degradation of the tumor suppressor p53. In addition, PE-46 inhibited the in vitro binding of E7 and Rb which is essential tumor suppressor for the control of cell cycle. The levels of mRNA for E6 and E7 were also decreased by PE-46. SiHa cells treated with PE-46 induced G0/G1 arrest, resulting in inhibition of growth. Our study showed that the PE-46 can inhibit the cervical carcinomas via both inhibition of bindings between oncogenes and tumor suppressors, and inhibition of G1longrightarrowS transition. PE-46 inhibited the oncogenecity of E6 and E7 of HPV 16 type, thus could be used as a putative modulating agent for the treatment of cervical carcinomas caused by HPV.
The hypochlorite ion ($OCl^-$) is a widely used disinfecting agent in pig rearing in Korea, but its residual effect on $CH_4$ production from pig slurry is unclear. The objective of this study was to investigate the inhibition effects of residual $OCl^-$ on $CH_4$ production during the initial anaerobic digestion stage of pig slurry. Three organic concentrations (9.9, 26.2 and 43.7 g/L) of volatile solids (VS) were tested with the addition of 52.3 mg/L $OCl^-$, ten times of the typical concentration used in Korea, or without $OCl^-$ (Control) in anaerobic batch culture. The culture was run under mesophilic ($38^{\circ}C$) conditions for 20 d. At the lowest organic concentration with $OCl^-$, the VS degradation was 10.3% lower (p<0.05) than Control, while at the higher organic concentration with $OCl^-$, it did not differ from Control. $CH_4$ yields were higher in the control treatments than their $OCl^-$ counterpart cultures, and $CH_4$ yields of Control and $OCl^-$ treatments at the organic concentrations of 9.9, 26.2 and 43.7 g/L differed in the probability level (p) of 0.31, 0.04, and 0.06, respectively. Additionally, $CH_4$ concentration increased steeply and reached 70.0% within 4 d in the absence $OCl^-$, but a gradual increase up to 60.0% was observed in 6 d in the $OCl^-$ treated cultures. The $R_m$ (the maximum specific $CH_4$ production rate) and ${\lambda}$ (lag phase time) of 9.9 g/L with $OCl^-$ were 8.1 ml/d and 25.6 d, while the $R_m$ was increased to 15.1 ml/d, and ${\lambda}$ was reduced to 11.4 d in PS-III (higher organic concentration) with $OCl^-$. The results suggest that a prolonged fermentation time was necessary for the methanogens to overcome the initial $OCl^-$ inhibitory effect, and an anaerobic reactor operated with high organic loadings was more advantageous to mitigate the inhibitory effect of residual hypochlorite ion.
Mobile IPv6 (MIPv6) enables a mobile node (MN) to maintain its connectivity with a correspondent node (CN) while changing its point of attachment. In MIPv6, packets sent from a CN to a MN during handover are lost. Several mechanisms including FMIPv6 and HMIPv6 have been proposed in order to minimize packet loss. However, such mechanisms still suffer from performance degradation due to not only packet loss but also out-of-sequence packets. In this paper, we propose I-FHMIPv6 to resolve packet loss as well as the out-of-sequence packet problem. In I-FHMIPv6, the flush message is newly defined in order to notify a home agent (HA) or CN of the fact that the binding cache entry of a MN is about to be updated. A MN receiving the flush message can know that there is no more packets transmitted via the previous route, which resolve the out-of-sequence packet problem. Moreover, with the proposed mechanism, we can minimize packet loss by integrating FMIPv6 and HMIPv6 efficiently. I-FHMIPv6 is evaluated by performing simulations, and the simulation results show that I-FHMIPv6 outperforms FMIPv6 and HMIPv6.
In the present study, the pro-apoptotic effects of methanol extract of Prunus mume fruits (MEPM) in human leukemia U937 cells were investigated. It was found that exposure to MEPM resulted in growth inhibition in a concentration-dependent manner by inducing apoptosis. The induction of apoptotic cell death in U937 cells by MEPM was correlated with a down-regulation of inhibitor of apoptosis protein (IAP) family, such as X-linked inhibitor of apoptosis protein (XIAP) and survivin, anti-apoptotic Bcl-2, up-regulation of FasL and cleavage of Bid. MEPM treatment also induced the proteolytic activation of caspase-3, caspase-8 and caspase-9, and degradation of caspase-3 substrate proteins, such as poly (ADP-ribose) polymerase (PARP) and ${\beta}$-catenin. In addition, apoptotic cell death induced by MEPM was significantly inhibited by z-DEVD-fmk, a caspase-3 specific inhibitor, which demonstrates the important role of caspase-3 in the apoptotic process by MEPM in U937 cells. Taken together, these findings suggest that P. mume extracts may be a potential chemotherapeutic agent for the control of human leukemia cells and further studies will be needed to identify the active compounds.
Some physico-chemical properties and biological activities of new fungicide formulations were tested to investigate a feasibility of water-floating formulation development for sheath blight control in rice. Pencycuron[1-(4-chlorobenzyl)-1-cyclopentyl-3-phenylurea] and flutolanil$({\alpha},{\alpha},{\alpha}$-trifluoro-3'-isopropoxy-O-toluanilide) were chosen as toxicants for the formulations. Vegetable oil and surface active agents were used as a floating agent and spreader, respectively. All the formulations tested showed an excellent spreadability on the water having over $35cm^2/mg$ and were chemically stable, which the degradation rates of active ingredients were less than 10% after 12 weeks of storage at $50^{\circ}C$. Most of the applied test formulation of pencycuron was retained within 0.5cm of the surface paddy water, while that of flutolanil was vertically dispersed in the water. Inhibition activity of the tested pencycuron formulation on the sclerotia germination of the pathogen in paddy water was maintained over 30 days after the formulation treatment. Control effect of 4% pencycuron water-floating formulated with surface active agent of hydro-lipophyllic balance 4.3 on the disease in rice was equal to the reference fungicide(pencycuron 25% WP) when the former was treated one day before the transplantation of rice seedlings. Overflowing the submerged paddy water after the formulation treatment resulted in a deterious effect on the disease control.
To evaluate the effects of microorganism agents on oil biodegradation, treatability and microcosm studies were conducted. Petroleum oil degrading bacteria were isolated from enriched cultures of oil-contaminated sediment samples using a mineral salts medium (MSM) containing 0.5% Arabian heavy crude oil as the sole carbon source. After a 5 day-incubation period using MSM, mixed microorganisms of three species (strains BS1, BS2 and BS4) degraded 48.4% of aliphatic hydrocarbons and 30.5% of aromatic hydrocarbons. Treatability and microcosm tests were performed in the three different treatment conditions (AO: Arabian heavy crude oil, AO+IN: Arabian heavy crude oil+inorganic nutrient, AO+IN+MM: Arabian heavy crude oil+inorganic nutrient+mixed microorganism agents). Among these, significantly enhanced biodegradation of aliphatic hydrocarbons were observed in AO+IN and AO+IN+MM conditions, without showing any different biodegradation rates in either condition. However, the degradation rates of aromatic hydrocarbons in an AO+IN+MM condition were increased by 50% in the treatability test and by 13% in the microcosm test compared to those in an AO+IN condition. Taken together, it can be concluded that mixed microorganism agents enhance the biodegradation of aliphatic and aromatic hydrocarbons in laboratory, a treatability test, and a microcosm test. This agent could especially be a useful tool in the application of bioremediation for removal of aromatic hydrocarbons.
Cervical cancer is one of the leading causes of female death from cancer worldwide with about 500,000 deaths per year. A strong association between certain human papilloma viruses (HPV types 16 and 18) and cervical cancer has been well known. An extract of natural products, named as Somatid, has been used to investigate whether this agent has the ability of inhibiting the oncogenes E6 and E7 of HPV type 16. This Somatid inhibited the proliferation of human cervical cancer cell lines (C-33A, SiHa, CaSki) and HaCaT keratinocytes in a dose response manner, In vitro binding assay and ELISA showed that Somatid inhibited the in vitro biding of E6 and E6AP which are essential for the binding and degradation of the tumor suppressor p53. In addition, Somatid inhibited the in vitro binding of E7 and Rb which is essential tumor suppressor for the control of cell cycle. The levels of mRNA for E6 and E7 were also decreased by Somatid. Our data suggested that Somatid inhibited the oncogenecity of E6 and E7 of HPV 16 type, thus can be used as a putative anti-HPV agent for the treatment of cervical carcinomas caused by HPV.
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