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Ko Nomura - One of the best experts on this subject based on the ideXlab platform.
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the education for sustainable Development Movement in japan a political perspective
Environmental Education Research, 2009Co-Authors: Ko NomuraAbstract:The Japanese government provided various political opportunities for non‐governmental groups and individuals in Japan to ‘jointly propose’ policy on education and sustainable Development at the World Summit on Sustainable Development, Johannesburg, 2002. These opportunities resulted in the emergence of the Japanese education for sustainable Development (ESD) Movement, and the crystallisation of a broader proposal that led to the initiation of the UN Decade of ESD (2005–2014). In this paper, we trace the history of these two outcomes, arguing that the opportunities, developed through the coordination of non‐governmental groups by government, took place within, rather than broadened or confronted, the government’s scope of interests. While the paper illustrates how the government’s continued support was crucial to the Development of the ESD Movement and the UN Decade, and the Movement has met with considerable achievements thus far (via its collective challenges to conventional education in a sustainability...
Song Hailong - One of the best experts on this subject based on the ideXlab platform.
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Proteomic Analysis and Biochemical Correlates of Mitochondrial Dysfunction after Low-Intensity Primary Blast Exposure
'Mary Ann Liebert Inc', 2019Co-Authors: Song Hailong, Chen Chen, Chen Mei, Cui Jiankun, Johnson, Catherine E., Cheng Jianlin, Wang Xiaowan, For Full List Of Authors, See Publisher\u27s Website.Abstract:Service members during military actions or combat training are frequently exposed to primary blasts by weaponry. Most studies have investigated moderate or severe brain injuries from blasts generating overpressures \u3e100 kPa, whereas understanding the pathophysiology of low-intensity blast (LIB)-induced mild traumatic brain injury (mTBI) leading to neurological deficits remains elusive. Our recent studies, using an open-field LIB-induced mTBI mouse model with a peak overpressure at 46.6 kPa, demonstrated behavioral impairments and brain nanoscale damages, notably mitochondrial and axonal ultrastructural changes. In this study, we used tandem mass tagged (TMT) quantitative proteomics and bioinformatics analysis to seek insights into the molecular mechanisms underlying ultrastructural pathology. Changes in global- and phospho-proteomes were determined at 3 and 24 h and at 7 and 30 days post injury (DPI), in order to investigate the biochemical and molecular correlates of mitochondrial dysfunction. Results showed striking dynamic changes in a total of 2216 proteins and 459 phosphorylated proteins at vary time points after blast. Disruption of key canonical pathways included evidence of mitochondrial dysfunction, oxidative stress, axonal/cytoskeletal/synaptic dysregulation, and neurodegeneration. Bioinformatic analysis identified blast-induced trends in networks related to cellular growth/Development/Movement/assembly and cell-to-cell signaling interactions. With observations of proteomic changes, we found LIB-induced oxidative stress associated with mitochondrial dysfunction mainly at 7 and 30 DPI. These dysfunctions included impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated respiration-relevant enzyme activities. Insights on the early pathogenesis of primary LIB-induced brain damage provide a template for further characterization of its chronic effects, identification of potential biomarkers, and targets for intervention
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Proteomic analysis and biochemical correlates of mitochondrial dysfunction following low-intensity primary blast exposure
2018Co-Authors: Song Hailong, Chen Chen, Chen Mei, Cui Jiankun, Cheng Jianlin, Wang Xiaowan, Johnson Catherine, Swerdlow, Russell H., Depalma Ralph, Xia WeimingAbstract:Service members during military actions or combat training are frequently exposed to primary blasts by weaponry. Most studies have investigated moderate or severe brain injuries from blasts generating overpressures over 100-kPa, while understanding the pathophysiology of low-intensity blast (LIB)-induced mild traumatic brain injury (mTBI) leading to neurological deficits remains elusive. Our recent studies, using an open-field LIB-induced mTBI mouse model with an peak overpressure at 46.6-kPa, demonstrated behavioral impairments and brain nanoscale damages, notably mitochondrial and axonal ultrastructural changes. In this study, we used tandem mass tagged (TMT) quantitative proteomics and bioinformatics analysis to seek insights into the molecular mechanisms underlying ultrastructural pathology. Changes in global- and phospho-proteomes were determined at 3 and 24 hours, 7 and 30 days post injury (DPI), and to investigate the biochemical and molecular correlates of mitochondrial dysfunction. Results showed striking dynamic changes in a total of 2216 global and 459 phosphorylated proteins at vary time points after blast. Disruption of key canonical pathways included evidence of mitochondrial dysfunction, oxidative stress, axonal/cytoskeletal/synaptic dysregulation, and neurodegeneration. Bioinformatic analysis identified blast induced trends in networks related to cellular growth/Development/Movement/assembly and cell-to-cell signaling interactions. With observations of proteomic changes, we found LIB-induced oxidative stress associated with mitochondrial dysfunction mainly at 7 and 30 DPI. These dysfunctions included impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated respiration-relevant enzyme activities. Insights on the early pahtogenesis of primary LIB-induced brain damage provide a template for further characterization of its chronic effects, identification of potential biomarkers and targets for intervention.Hailong song (1), Mei Chen (6), Chen Chen (2), Jiankun Cui (1,7), Catherine Johnson (3), Jianlin Cheng (2), Xiaowan Wang (4), Russell H. Swerdlow (4), Ralph DePalma (5), Weiming Xia (6), Zezong Gu (1,7) ; 1. Department of Pathology & Anatomical Sciences, University of Missouri School of Medicine; 2. Department of Computer Sciences, University of Missouri; 3. Department of Mining and Nuclear Engineering, Missouri University of Science and Technology; 4. Department of Neurology, University of Kansas Medical Center; 5. Office of Research and Development, Department of Veterans Affairs; 6. Bedford VA Medical Center; 7. Truman VA Hospital Research Servic
Chen Chen - One of the best experts on this subject based on the ideXlab platform.
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Proteomic Analysis and Biochemical Correlates of Mitochondrial Dysfunction after Low-Intensity Primary Blast Exposure
'Mary Ann Liebert Inc', 2019Co-Authors: Song Hailong, Chen Chen, Chen Mei, Cui Jiankun, Johnson, Catherine E., Cheng Jianlin, Wang Xiaowan, For Full List Of Authors, See Publisher\u27s Website.Abstract:Service members during military actions or combat training are frequently exposed to primary blasts by weaponry. Most studies have investigated moderate or severe brain injuries from blasts generating overpressures \u3e100 kPa, whereas understanding the pathophysiology of low-intensity blast (LIB)-induced mild traumatic brain injury (mTBI) leading to neurological deficits remains elusive. Our recent studies, using an open-field LIB-induced mTBI mouse model with a peak overpressure at 46.6 kPa, demonstrated behavioral impairments and brain nanoscale damages, notably mitochondrial and axonal ultrastructural changes. In this study, we used tandem mass tagged (TMT) quantitative proteomics and bioinformatics analysis to seek insights into the molecular mechanisms underlying ultrastructural pathology. Changes in global- and phospho-proteomes were determined at 3 and 24 h and at 7 and 30 days post injury (DPI), in order to investigate the biochemical and molecular correlates of mitochondrial dysfunction. Results showed striking dynamic changes in a total of 2216 proteins and 459 phosphorylated proteins at vary time points after blast. Disruption of key canonical pathways included evidence of mitochondrial dysfunction, oxidative stress, axonal/cytoskeletal/synaptic dysregulation, and neurodegeneration. Bioinformatic analysis identified blast-induced trends in networks related to cellular growth/Development/Movement/assembly and cell-to-cell signaling interactions. With observations of proteomic changes, we found LIB-induced oxidative stress associated with mitochondrial dysfunction mainly at 7 and 30 DPI. These dysfunctions included impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated respiration-relevant enzyme activities. Insights on the early pathogenesis of primary LIB-induced brain damage provide a template for further characterization of its chronic effects, identification of potential biomarkers, and targets for intervention
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Analysis of a novel mutant allele of GSL8 reveals its key roles in cytokinesis and symplastic trafficking in Arabidopsis
BMC, 2018Co-Authors: Behnaz Saatian, Ryan S. Austin, Gang Tian, Chen Chen, Vi Nguyen, Susanne E. Kohalmi, Danny Geelen, Yuhai CuiAbstract:Abstract Background Plant cell walls are mainly composed of polysaccharides such as cellulose and callose. Callose exists at a very low level in the cell wall; however, it plays critical roles at different stages of plant Development as well as in defence against unfavorable conditions. Callose is accumulated at the cell plate, at plasmodesmata and in male and female gametophytes. Despite the important roles of callose in plants, the mechanisms of its synthesis and regulatory properties are not well understood. Results CALLOSE SYNTHASE (CALS) genes, also known as GLUCAN SYNTHASE-LIKE (GSL), comprise a family of 12 members in Arabidopsis thaliana. Here, we describe a new allele of GSL8 (named essp8) that exhibits pleiotropic seedling defects. Reduction of callose deposition at the cell plates and plasmodesmata in essp8 leads to ectopic endomitosis and an increase in the size exclusion limit of plasmodesmata during early seedling Development. Movement of two non-cell-autonomous factors, SHORT ROOT and microRNA165/6, both required for root radial patterning during embryonic root Development, are dysregulated in the primary root of essp8. This observation provides evidence for a molecular mechanism explaining the gsl8 root phenotype. We demonstrated that GSL8 interacts with PLASMODESMATA-LOCALIZED PROTEIN 5, a β-1,3-glucanase, and GSL10. We propose that they all might be part of a putative callose synthase complex, allowing a concerted regulation of callose deposition at plasmodesmata. Conclusion Analysis of a novel mutant allele of GSL8 reveals that GSL8 is a key player in early seedling Development in Arabidopsis. GSL8 is required for maintaining the basic ploidy level and regulating the symplastic trafficking. Callose deposition at plasmodesmata is highly regulated and occurs through interaction of different components, likely to be incorporated into a callose biosynthesis complex. We are providing new evidence supporting an earlier hypothesis that GSL8 might have regulatory roles apart from its enzymatic function in plasmodesmata regulation
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Proteomic analysis and biochemical correlates of mitochondrial dysfunction following low-intensity primary blast exposure
2018Co-Authors: Song Hailong, Chen Chen, Chen Mei, Cui Jiankun, Cheng Jianlin, Wang Xiaowan, Johnson Catherine, Swerdlow, Russell H., Depalma Ralph, Xia WeimingAbstract:Service members during military actions or combat training are frequently exposed to primary blasts by weaponry. Most studies have investigated moderate or severe brain injuries from blasts generating overpressures over 100-kPa, while understanding the pathophysiology of low-intensity blast (LIB)-induced mild traumatic brain injury (mTBI) leading to neurological deficits remains elusive. Our recent studies, using an open-field LIB-induced mTBI mouse model with an peak overpressure at 46.6-kPa, demonstrated behavioral impairments and brain nanoscale damages, notably mitochondrial and axonal ultrastructural changes. In this study, we used tandem mass tagged (TMT) quantitative proteomics and bioinformatics analysis to seek insights into the molecular mechanisms underlying ultrastructural pathology. Changes in global- and phospho-proteomes were determined at 3 and 24 hours, 7 and 30 days post injury (DPI), and to investigate the biochemical and molecular correlates of mitochondrial dysfunction. Results showed striking dynamic changes in a total of 2216 global and 459 phosphorylated proteins at vary time points after blast. Disruption of key canonical pathways included evidence of mitochondrial dysfunction, oxidative stress, axonal/cytoskeletal/synaptic dysregulation, and neurodegeneration. Bioinformatic analysis identified blast induced trends in networks related to cellular growth/Development/Movement/assembly and cell-to-cell signaling interactions. With observations of proteomic changes, we found LIB-induced oxidative stress associated with mitochondrial dysfunction mainly at 7 and 30 DPI. These dysfunctions included impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated respiration-relevant enzyme activities. Insights on the early pahtogenesis of primary LIB-induced brain damage provide a template for further characterization of its chronic effects, identification of potential biomarkers and targets for intervention.Hailong song (1), Mei Chen (6), Chen Chen (2), Jiankun Cui (1,7), Catherine Johnson (3), Jianlin Cheng (2), Xiaowan Wang (4), Russell H. Swerdlow (4), Ralph DePalma (5), Weiming Xia (6), Zezong Gu (1,7) ; 1. Department of Pathology & Anatomical Sciences, University of Missouri School of Medicine; 2. Department of Computer Sciences, University of Missouri; 3. Department of Mining and Nuclear Engineering, Missouri University of Science and Technology; 4. Department of Neurology, University of Kansas Medical Center; 5. Office of Research and Development, Department of Veterans Affairs; 6. Bedford VA Medical Center; 7. Truman VA Hospital Research Servic
Maria Graca Carvalho - One of the best experts on this subject based on the ideXlab platform.
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new and renewable energy technologies for sustainable Development proceedings of the conference on new and renewable energy technologies for sustainable Development 24 26 june 2002 ponta delgada azores portugal
2004Co-Authors: Naim Afgan, Maria Graca CarvalhoAbstract:The International Conference on New and Renewable Energy Technologies for Sustainable Development held in Ponta Delgada, Azores (2002), Portugal, has provided technology specialists and hardware developers with the opportunity to discuss, review and demonstrate the research directions, the design methodologies, and the production techniques leading to cost- effective energy technologies for sustainable Development. This dialog provides the context for more detailed technical presentations and panel discussions on energy systems, renewable resource exploitation, and the engineering design and optimisation for minimum resource consumption. The papers included in this volume are selected from those presented at the conference reflecting to present the state-of-the-art Developments in the field. The selection of papers presented in this volume has enlightened various fields of scientific and economic Development which should merge efforts in the understanding of the sustainable Development concept and technological implications. The book will be of particular interest to engineering practitioners, product developers, researchers, and also economists, political scientists and government administrators exploring the multifaceted relationship between renewable energy technologies and sustainable Development. Keynote lectures frame the technical and policy issues confronting the sustainable Development Movement and enrich the dialog between various segments of the community.
For Full List Of Authors, See Publisher\u27s Website. - One of the best experts on this subject based on the ideXlab platform.
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Proteomic Analysis and Biochemical Correlates of Mitochondrial Dysfunction after Low-Intensity Primary Blast Exposure
'Mary Ann Liebert Inc', 2019Co-Authors: Song Hailong, Chen Chen, Chen Mei, Cui Jiankun, Johnson, Catherine E., Cheng Jianlin, Wang Xiaowan, For Full List Of Authors, See Publisher\u27s Website.Abstract:Service members during military actions or combat training are frequently exposed to primary blasts by weaponry. Most studies have investigated moderate or severe brain injuries from blasts generating overpressures \u3e100 kPa, whereas understanding the pathophysiology of low-intensity blast (LIB)-induced mild traumatic brain injury (mTBI) leading to neurological deficits remains elusive. Our recent studies, using an open-field LIB-induced mTBI mouse model with a peak overpressure at 46.6 kPa, demonstrated behavioral impairments and brain nanoscale damages, notably mitochondrial and axonal ultrastructural changes. In this study, we used tandem mass tagged (TMT) quantitative proteomics and bioinformatics analysis to seek insights into the molecular mechanisms underlying ultrastructural pathology. Changes in global- and phospho-proteomes were determined at 3 and 24 h and at 7 and 30 days post injury (DPI), in order to investigate the biochemical and molecular correlates of mitochondrial dysfunction. Results showed striking dynamic changes in a total of 2216 proteins and 459 phosphorylated proteins at vary time points after blast. Disruption of key canonical pathways included evidence of mitochondrial dysfunction, oxidative stress, axonal/cytoskeletal/synaptic dysregulation, and neurodegeneration. Bioinformatic analysis identified blast-induced trends in networks related to cellular growth/Development/Movement/assembly and cell-to-cell signaling interactions. With observations of proteomic changes, we found LIB-induced oxidative stress associated with mitochondrial dysfunction mainly at 7 and 30 DPI. These dysfunctions included impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated respiration-relevant enzyme activities. Insights on the early pathogenesis of primary LIB-induced brain damage provide a template for further characterization of its chronic effects, identification of potential biomarkers, and targets for intervention