This article presents a community learning model formulated by Engineers Without Borders Colombia with the aim of providing communities with tools to create sustainable productive solutions which have relevancy for members and for potential customers. The goal of this formulation is to promote learning processes that are guided by decisions made by community members to propose sustainable and replicable initiatives. The model applicability is evidenced through a case study devoted to strengthening community-led green businesses in the Guavio Province, Colombia by collecting lessons and conclusions. Ultimately, this collection will prove useful in replicating the learning model in other similar rural communities.
In this experiment, using the methods of drought-stress in the pot and PEG simulative drought-stress, three native rocky-slope grasses Pogonatherum panideum(Lam.) Hack, Erioophorum comosum nees and Cynodon dactylon cultivated in the pots were selected as materials to study their drought-resistance by analyzing the indexes such as the leaf area index, the drying roots accumulation, the holding water ability of leaf, the relative conductance of leaf, the soluble protein, chlorophyll. At the same time, by comparing with membership function value of each index, the order of each grass drought-resistance was decided. The results showed that the drought-resistance of Erioophorum comosum nees was stronger than Cynodon dactylon and drought-resistance of Cynodon dactylon was stronger than Pogonatherum panideum (Lam.) Hack. The purpose of the experimental results was to find theoretical foundations for selecting and cultivating native protecting-slope vegetations to adapt to rocky slopes. 相似文献
Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1. 相似文献