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J. H. Fleurke-Rozema L. van Leijden K. van de Kamp E. Pajkrt C. M. Bilardo R. J. M. Snijders 《黑龙江环境通报》2015,35(5):483-485
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Joyeeta Gupta Catrien Termeer Judith Klostermann Sander Meijerink Margo van den Brink Pieter Jong Sibout Nooteboom Emmy Bergsma 《Environmental Science & Policy》2010,13(6):459-471
Climate change potentially brings continuous and unpredictable changes in weather patterns. Consequently, it calls for institutions that promote the adaptive capacity of society and allow society to modify its institutions at a rate commensurate with the rate of environmental change. Institutions, traditionally conservative and reactive, will now have to support social actors to proactively respond through planned processes and deliberate steps, but also through cherishing and encouraging spontaneous and autonomous change, as well as allowing for institutional redesign. This paper addresses the question: How can the inherent characteristics of institutions to stimulate the capacity of society to adapt to climate change from local through to national level be assessed? On the basis of a literature review and several brainstorm sessions, this paper presents six dimensions: Variety, learning capacity, room for autonomous change, leadership, availability of resources and fair governance. These dimensions and their 22 criteria form the Adaptive Capacity Wheel. This wheel can help academics and social actors to assess if institutions stimulate the adaptive capacity of society to respond to climate change; and to focus on whether and how institutions need to be redesigned. This paper also briefly demonstrates the application of this Adaptive Capacity Wheel to different institutions. 相似文献
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L. E. M. Niers J. A. M. Smeitink J. M. F. Trijbels R. C. A. Sengers A. J. M. Janssen L. P. van den Heuvel 《黑龙江环境通报》2001,21(10):871-880
NADH:ubiquinone oxidoreductase (complex I of the mitochondrial respiratory chain) deficiency is a severe disorder with an often early fatal outcome. Prenatal diagnosis for complex I defects currently relies mainly on biochemical assays of complex I in fetal tissues such as chorionic villi (CV), and is only in a minority of cases possible by means of mutational analysis of nuclear-encoded genes of complex I. We report on our experience to date with prenatal diagnosis in pregnancies at risk for complex I deficiency. We measured complex I activity in native CV and/or cultured CV in 23 pregnancies in 15 families. In accordance with the results of the investigations in CV, 15 children were born clinically unaffected. Two prenatally diagnosed unaffected fetuses and two prenatally diagnosed affected fetuses were lost prematurely with spontaneous or provoked abortions, respectively. Two affected children were born (prenatally found to be affected). In two pregnancies a discrepancy between native and cultured cells was found. We conclude that prenatal diagnosis for complex I deficiency can be reliably performed. Pitfalls were encountered in using cultured CV as a result of maternal cell contamination (MCC). Future research on pathogenic nuclear mutations underlying complex I deficiency will extend the possibilities for prenatal diagnosis at the molecular level. Copyright © 2001 John Wiley & Sons, Ltd. 相似文献
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