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Articles by Ping Shi
Total Records ( 3 ) for Ping Shi
  Qiuying Han , Xiaoping Huang , Qianguo Xing and Ping Shi
  The coastal sea of South China provided an important habitat for protection and propagation of marine organisms. Rapid economic development and human activities, such as wastewater discharge, reclamation, overfishing and aquaculture in the South China Sea had already resulted in environmental degradation, and thus caused sharp contradictions between exploitation and protection of the coastal sea of South China. In this present article, the main environment problems and degradation trends were reviewed based on literatures and other sources of information, which mainly referenced nutrient pollution, persistent organic pollution and metal pollution, decrease of biodiversity, reduction of marine habitat and frequent natural and ecological disasters. The current efforts in China on protecting the environment in the coastal sea of South China were discussed, which included improving legislation by formulating a series of laws and regulations at national or local level, setting up natural reserves, and supporting research projects. There were many challenges regarding policy, management and science research to protect and sustain the coastal sea of South China, such as imperfect legal and administrative systems, lack of public participation, poor financial support and lack of monitoring and evaluation. Finally, some recommendations were put forward for the sake of the sustainable use of the environment in the coastal sea of South China, including reinforcing the planning of marine resource exploitation and use through integrated coastal zone management, strengthening the marine environment and protection awareness of the public, and scientifically establishing the fishery spawning spots and aquatic reserves.
  Qianguo Xing , Hubert Loisel , Francois G. Schmitt , David Dessailly , Yanju Hao , Qiuying Han and Ping Shi
  Time series of chlorophyll-a concentration (chl a), backscattering coefficient at 490 nm (b bp(490)) and spectral slope of b bp (?) derived from satellite imagery of ocean color were used to study the aquatic ecosystem of the Southern Yellow Sea during the time period of 1997–2007. Our study indicated that chl a increased in offshore waters by 0.02 mg m-3 y -1 (p < 0.05), in contrast to a decline observed in the middle and low-latitude global waters. b bp(490), a proxy of total suspended particulate matter concentration did not have any significant trend, while ?, a proxy of the relative proportion of small-sized and larger particles in the surface ocean, decreased significantly. Annual spring phytoplankton blooms occurred in nearshore and offshore waters of the central Southern Yellow Sea; while autumn blooms only occurred in nearshore waters.
  Anna- Lena Strom , Ping Shi , Fujian Zhang , Jozsef Gal , Renee Kilty , Lawrence J. Hayward and Haining Zhu
  An important consequence of protein misfolding related to neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), is the formation of proteinaceous inclusions or aggregates within the central nervous system. We have previously shown that several familial ALS-linked copper-zinc superoxide dismutase (SOD1) mutants (A4V, G85R, and G93A) interact and co-localize with the dynein-dynactin complex in cultured cells and affected tissues of ALS mice. In this study, we report that the interaction between mutant SOD1 and the dynein motor plays a critical role in the formation of large inclusions containing mutant SOD1. Disruption of the motor by overexpression of the p50 subunit of dynactin in neuronal and non-neuronal cell cultures abolished the association between aggregation-prone SOD1 mutants and the dynein-dynactin complex. The p50 overexpression also prevented mutant SOD1 inclusion formation and improved the survival of cells expressing A4V SOD1. Furthermore, we observed that two ALS-linked SOD1 mutants, H46R and H48Q, which showed a lower propensity to interact with the dynein motor, also produced less aggregation and fewer large inclusions. Overall, these data suggest that formation of large inclusions depends upon association of the abnormal SOD1s with the dynein motor. Whether the misfolded SOD1s directly perturb axonal transport or impair other functional properties of the dynein motor, this interaction could propagate a toxic effect that ultimately causes motor neuron death in ALS.
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