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Sustainable Development of Indonesia`s Agricultural Sector
( Eng Seng Chia ),( Dongyu Li ),( Xutong Ma ),( Jixi Wang ),( Yiting Wang ),( Jiaxu Zhu ) 한국시스템다이내믹스학회 2016 한국시스템다이내믹스 연구 Vol.17 No.4
The Indonesian agricultural output has been struggling to provide for the demand of the rising population in recent years owing to the sluggish growth rate in this sector as compared to the overall performance of the economy. While the current slash-and-burn technique widely employed by Indonesian peasants is able to boost the output in the short term, its negative implications on the environment and the constraints in available forest area casts doubts to its sustainability in the long run. As the results from our iThink model simulation has illustrated, the output will cease increasing and decline in about 90 years” time due to the drastic drop in forest coverage. Based on the sensitivity analysis of the affecting factors, three policy amendments are proposed to avert the gloomy perspective, namely increasing funding for Research and Development, curbing burning activities, and actively returning abandoned land to forests. With the effective implementation of the suggested policies, the growth in the agricultural sector will be steered back to a sustainable track, which is further confirmed by the model projection.
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( Hongtao Liu ),( Seng Zhu ),( Yingying Sun ),( Na Li ),( Jingmin Gu ),( Changjiang Sun ),( Xin Feng ),( Wenyu Han ),( Jianxia Jiang ),( Liancheng Lei ) 한국미생물 · 생명공학회 2017 Journal of microbiology and biotechnology Vol.27 No.1
Meningitis caused by Streptococcus suis serotype 2 (S. suis 2) is a great threat to the pig industry and human health. Virulence factors associated with the pathogenesis of meningitis have yet to be clearly defined, even though many potential S. suis 2 virulence factors have been identified. This greatly hinders the progress of S. suis 2 meningitis pathogenesis research. In this study, a co-culture blood-brain barrier (BBB) model was established using primary porcine brain microvascular endothelial cells and astrocytes, and the whole genome library of S. suis 2 was constructed using phage display technology. Finally, a total of 14 potential virulence factors contributing to S. suis 2 adherence to and invasion of the BBB were selected by analyzing the interactions between the phage library and the co-culture model. Twelve of these factors have not been previously reported in meningitis-related research. The data provide valuable insight into the pathogenesis of S. suis 2 meningitis and potential targets for the development of drug therapies.
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You-Sun Kim,Seng-Jin Choi,Jun-Pyo Choi,전성규,이병재,고용송,이춘근,Jack A. Elias,Yoon-Keun Kim,Sun-Young Oh,Zhou Zhu 생화학분자생물학회 2010 Experimental and molecular medicine Vol.42 No.8
IL-4 and IL-13 are closely related cytokines that are produced by Th2 cells. However, IL-4 and IL-13 have different effects on the development of asthma phenotypes. Here, we evaluated downstream molecular mechanisms involved in the development of Th2 type asthma phenotypes. A murine model of Th2 asthma was used that involved intraperitoneal sensitization with an allergen (ovalbumin) plus alum and then challenge with ovalbumin alone. Asthma phenotypes, including airway-hyperresponsiveness (AHR), lung inflammation,and immunologic parameters were evaluated after allergen challenge in mice deficient in candidate genes. The present study showed that methacholine AHR and lung inflammation developed in allergen-challenged IL-4-deficient mice but not in allergen-challenged IL-13-deficient mice. In addition, the production of OVA-specific IgG2a and IFN-γ-inducible protein (IP)-10was also impaired in the absence of IL-13, but not of IL-4. Lung-targeted IFN-γ over-expression in the airways enhanced methacholine AHR and non-eosinophilic inflammation; in addition, these asthma phenotypes were impaired in allergen-challenged IFN-γ-deficient mice. Moreover, AHR, non-eosinophilic inflammation,and IFN-γ expression were impaired in allergen-challenged IL-12Rβ2- and STAT4-deficient mice; however, AHR and non-eosinophilic inflammation were not impaired in allergen-challenged IL-4Rα-deficient mice, and these phenomena were accompanied by the enhanced expression of IL-12 and IFN-γ. The present data suggest that IL-13-mediated asthma phenotypes, such as AHR and non-eosinophilic inflammation, in the Th2 type asthma are dependent on the IL-12-STAT4-IFN-γ axis, and that these asthma phenotypes are independent of IL-4Ralpha-mediated signaling.
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Kim, You-Sun,Choi, Seng-Jin,Choi, Jun-Pyo,Jeon, Seong-Gyu,Oh, Sun-Young,Lee, Byung-Jae,Gho, Yong-Song,Lee, Chun-Geun,Zhu, Zhou,Elias, Jack A.,Kim, Yoon-Keun Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.8
IL-4 and IL-13 are closely related cytokines that are produced by Th2 cells. However, IL-4 and IL-13 have different effects on the development of asthma phenotypes. Here, we evaluated downstream molecular mechanisms involved in the development of Th2 type asthma phenotypes. A murine model of Th2 asthma was used that involved intraperitoneal sensitization with an allergen (ovalbumin) plus alum and then challenge with ovalbumin alone. Asthma phenotypes, including airway- hyperresponsiveness (AHR), lung inflammation, and immunologic parameters were evaluated after allergen challenge in mice deficient in candidate genes. The present study showed that methacholine AHR and lung inflammation developed in allergen-challenged IL-4-deficient mice but not in allergen-challenged IL-13-deficient mice. In addition, the production of OVA-specific IgG2a and IFN-${\gamma}$-inducible protein (IP)-10 was also impaired in the absence of IL-13, but not of IL-4. Lung-targeted IFN-${\gamma}$ over-expression in the airways enhanced methacholine AHR and non-eosinophilic inflammation; in addition, these asthma phenotypes were impaired in allergen-challenged IFN-${\gamma}$-deficient mice. Moreover, AHR, non-eosinophilic inflammation, and IFN-${\gamma}$ expression were impaired in allergen- challenged IL-$12R{\beta}2$- and STAT4-deficient mice; however, AHR and non-eosinophilic inflammation were not impaired in allergen-challenged IL-$4R{\alpha}$-deficient mice, and these phenomena were accompanied by the enhanced expression of IL-12 and IFN-${\gamma}$. The present data suggest that IL-13-mediated asthma phenotypes, such as AHR and non-eosinophilic inflammation, in the Th2 type asthma are dependent on the IL-12-STAT4-IFN-${\gamma}$ axis, and that these asthma phenotypes are independent of IL-4Ralpha-mediated signaling.
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