Promoting Entrepreneurship through a Community Learning Model – Case Study: Green Businesses

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.

     

The life span of the biosphere revisited

A decade ago, Lovelock and Whitfield raised the question of how much longer the biosphere can survive on Earth. They pointed out that, despite the current fossil-fuel induced increase in the atmospheric CO2 concentration, the long-term trend should be in the opposite direction: as increased solar luminosity warms the Earth, silicate rocks should weather more readily, causing atmospheric CO2 to decrease. In their model, atmospheric CO2 falls below the critical level for C3 photosynthesis, 150 parts per million (p.p.m.), in only 100 Myr, and this is assumed to mark the demise of the biosphere as a whole. Here, we re-examine this problem using a more elaborate model that includes a more accurate treatment of the greenhouse effect of CO2, a biologically mediated weathering parameterization, and the realization that C4 photosynthesis can persist to much lower concentrations of atmospheric CO2(<10 p.p.m.). We find that a C4-plant-based biosphere could survive for at least another 0.9 Gyr to 1.5 Gyr after the present time, depending respectively on whether CO2 or temperature is the limiting factor. Within an additional 1 Gyr, Earth may lose its water to space, thereby following the path of its sister planet, Venus.     

白莲河水电厂2号机组振动在线监测系统

在线监测系统是水电机组安全运行的保证，该系统能监视机组的运行情况，对尾水管压力脉动值、顶盖、机架跳动及主轴摆度值进行适时测量．为推广该成果的应用，论述了白莲河水电厂振动在线监测系统的设计方法和系统具备的功能．     

烃源岩中烷基二苯并噻吩组成及其地球化学意义

对一个海相地层的实际剖面进行了研究，发现烃源岩芳烃馏分中烷基二苯并噻吩和烷基苯并萘噻吩的相对丰度与碳酸盐矿物含量间有良好的正相关性．不同岩性中含硫芳烃相对丰度的变化顺序是：碳酸盐岩＞泥灰岩＞泥质岩．在深度剖面上，二苯并噻吩（ＤＢＴ）与甲基二苯并噻吩（ＭＤＢＴ）呈消长关系。４－ＭＤＢＴ和２＋３－ＭＤＢＴ的相对丰度随埋深增加而增加．１－ＭＤＢＴ则随之下降，４－ＭＤＢＴ／１－ＭＤＢＴ值和２＋３－ＭＤＢＴ／１－ＭＤＢＴ值能较好地反映有机质的热演化程度．     

太平沟大桥曲线箱梁顶推施工设计概述

太平沟大桥该桥全长358．8m，平面位于R=1380．965m圆曲线及L5=300m的缓和曲线上，是国内曲线连续顶推桥长最长、跨径最大的一座桥。详细介绍了太平沟大桥曲线箱梁顶推设计特点及施工设计要点。     

Termination of asymmetric cell division and differentiation of stomata

Stomata consist of a pair of guard cells that mediate gas and water-vapour exchange between plants and the atmosphere. Stomatal precursor cells-meristemoids-possess a transient stem-cell-like property and undergo several rounds of asymmetric divisions before further differentiation. Here we report that the Arabidopsis thaliana basic helix-loop-helix (bHLH) protein MUTE is a key switch for meristemoid fate transition. In the absence of MUTE, meristemoids abort after excessive asymmetric divisions and fail to differentiate stomata. Constitutive overexpression of MUTE directs the entire epidermis to adopt guard cell identity. MUTE has two paralogues: FAMA, a regulator of guard cell morphogenesis, and SPEECHLESS (SPCH). We show that SPCH directs the first asymmetric division that initiates stomatal lineage. Together, SPCH, MUTE and FAMA bHLH proteins control stomatal development at three consecutive steps: initiation, meristemoid differentiation and guard cell morphogenesis. Our findings highlight the roles of closely related bHLHs in cell type differentiation in plants and animals.     

Oxysterols direct immune cell migration via EBI2

Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) is a G-protein-coupled receptor that is required for humoral immune responses; polymorphisms in the receptor have been associated with inflammatory autoimmune diseases. The natural ligand for EBI2 has been unknown. Here we describe the identification of 7α,25-dihydroxycholesterol (also called 7α,25-OHC or 5-cholesten-3β,7α,25-triol) as a potent and selective agonist of EBI2. Functional activation of human EBI2 by 7α,25-OHC and closely related oxysterols was verified by monitoring second messenger readouts and saturable, high-affinity radioligand binding. Furthermore, we find that 7α,25-OHC and closely related oxysterols act as chemoattractants for immune cells expressing EBI2 by directing cell migration in vitro and in vivo. A critical enzyme required for the generation of 7α,25-OHC is cholesterol 25-hydroxylase (CH25H). Similar to EBI2 receptor knockout mice, mice deficient in CH25H fail to position activated B cells within the spleen to the outer follicle and mount a reduced plasma cell response after an immune challenge. This demonstrates that CH25H generates EBI2 biological activity in vivo and indicates that the EBI2-oxysterol signalling pathway has an important role in the adaptive immune response.     

Shank3 mutant mice display autistic-like behaviours and striatal dysfunction

Autism spectrum disorders (ASDs) comprise a range of disorders that share a core of neurobehavioural deficits characterized by widespread abnormalities in social interactions, deficits in communication as well as restricted interests and repetitive behaviours. The neurological basis and circuitry mechanisms underlying these abnormal behaviours are poorly understood. SHANK3 is a postsynaptic protein, whose disruption at the genetic level is thought to be responsible for the development of 22q13 deletion syndrome (Phelan-McDermid syndrome) and other non-syndromic ASDs. Here we show that mice with Shank3 gene deletions exhibit self-injurious repetitive grooming and deficits in social interaction. Cellular, electrophysiological and biochemical analyses uncovered defects at striatal synapses and cortico-striatal circuits in Shank3 mutant mice. Our findings demonstrate a critical role for SHANK3 in the normal development of neuronal connectivity and establish causality between a disruption in the Shank3 gene and the genesis of autistic-like behaviours in mice.