162 research outputs found

    Biodiversity Research for Sustainable Development: Can It Be Achieved?

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    Biodiversity is said to be the "heart of sustainable agricultural systems". Biodiversity research is envisioned to provide a better understanding of development issues so that better policy responses, management practices and actions will ultimately redound to a better quality of life for all, especially the poor. It is in this light that the Philippines-Netherlands Biodiversity Research Programme for Development is revisited and analyzed in this paper. This and other similar projects provide lessons for capacity development at the community, national, regional and international levels. To proceed with its analysis, the paper fleshes out the framework of sustainable development, situating the role of biodiversity in determining the pathway of development. As shown, biodiversity, as an element of the natural resource base, and in concert with technology and sociocultural factors, will continue to be relevant in a rapidly changing and increasingly globalized world. It also presents the sustainable livelihood framework to illustrate that biodiversity alone, being only one component of natural capital, cannot alleviate poverty if nothing is done with the other capital assets. One important lesson gleaned from the analysis of biodiversity research is that not all biodiversity is good. The key is to better understand the interactions between various levels and how these can be harnessed into positive interactions to produce a productive, stable and sustainable resource base. Another emerging lesson is that biodiversity can be conserved in agroecosystems if the poor resource users can be enabled to use it to improve their assets in the context of the sustainable livelihood framework. The effective management and conservation of agricultural biodiversity can be achieved through product value addition and link to market, germplasm enhancement, and participatory plant breeding, among others.biodiversity, sustainable development, agroecosystems

    GUCY2C Opposes Premalignant Transformation in Intestine by Regulating PTEN-PI3K/AKT Signaling

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    An evolving paradigm expanding the genetic basis of cancer suggests that tissue-specific developmental programs indelibly imprint restricted repertoires governing homeostasis, forming the substrate for lineage-dependent tumor induction by dysregulation of survival pathways. GUCY2C, the intestinal receptor for the paracrine hormones guanylin and uroguanylin whose early loss characterizes transformation, has emerged as a component of developmental programs organizing spatiotemporal patterning along the crypt-surface axis whose dysregulation promotes hyperproliferation and genetic instability underlying neoplasia. Here we identify GUCY2C as a reversible switch for lineage-dependent tumorigenesis whose disruption amplifies survival circuits essential for regenerative homeostasis and required for transformation. Elimination of GUCY2C in mice expands proliferating crypts, accelerating the cell cycle at the G1/S transition. Proliferative induction is coupled with altered metabolic programming, with an increase in aerobic glycolysis and a reciprocal reduction in mitochondrial biogenesis and oxidative phosphorylation, recapitulating the metabolic phenotype of human tumors. Conversely, GUCY2C signaling restores homeostatic circuits in colon cancer cells, decelerating the cell cycle and switching ATP production from glycolysis to mitochondrial metabolism, recapitulating normal enterocytes. Moreover, oral administration of the downstream mediator of GUCY2C signaling, cyclic GMP, reverses crypt hyperplasia and restores normal proliferative and metabolic programs in mice deficient in GUCY2C. Coordination of survival circuits by GUCY2C is orchestrated through the oncogene AKT, whose inhibition mimics, and activation eliminates, GUCY2C regulation of proliferation and metabolism. Modulation of AKT signaling by GUCY2C is, in part, mediated by the tumor suppressor, PTEN. Silencing PTEN eliminates GUCY2C regulation of AKT, proliferation and metabolism. Thus, disruption of developmentally restricted signaling by GUCY2C, reflecting loss of paracrine hormones, induces maladaptive survival pathways underlying crypt-surface homeostasis whose tissue-specific deregulation contributes to lineage dependency in intestinal tumorigenesis. With the role of guanylin and uroguanylin loss in transformation, the universal compensatory over-expression of GUCY2C by colorectal tumors offers a unique therapeutic opportunity for cancer prevention through oral hormone replacement therapy

    The Effect of Innovation on Industrial Value-added in China

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    China has achieved great economic growth since the reform in 1978. China’s industry has been developed significantly along with the economic advancement during the decades. The innovation has been argued by researchers to contribute to the economic growth. Since the industry output grows and contributes to the Chinese economic performance, the issue about how the innovation affects the industry in China deserves exploration. The granted patent has been always an indicator of the level of technological innovation in a country. The author intends to explore the extent that the innovations effect the value-added of industries in China. The main approach is to analyze the econometric relationship between the annual amounts of granted patents and the annual value-added per capita among various industrial sectors in China between 1986 and 2006

    HL-Pow: A Learning-Based Power Modeling Framework for High-Level Synthesis

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    High-level synthesis (HLS) enables designers to customize hardware designs efficiently. However, it is still challenging to foresee the correlation between power consumption and HLS-based applications at an early design stage. To overcome this problem, we introduce HL-Pow, a power modeling framework for FPGA HLS based on state-of-the-art machine learning techniques. HL-Pow incorporates an automated feature construction flow to efficiently identify and extract features that exert a major influence on power consumption, simply based upon HLS results, and a modeling flow that can build an accurate and generic power model applicable to a variety of designs with HLS. By using HL-Pow, the power evaluation process for FPGA designs can be significantly expedited because the power inference of HL-Pow is established on HLS instead of the time-consuming register-transfer level (RTL) implementation flow. Experimental results demonstrate that HL-Pow can achieve accurate power modeling that is only 4.67% (24.02 mW) away from onboard power measurement. To further facilitate power-oriented optimizations, we describe a novel design space exploration (DSE) algorithm built on top of HL-Pow to trade off between latency and power consumption. This algorithm can reach a close approximation of the real Pareto frontier while only requiring running HLS flow for 20% of design points in the entire design space.</p

    Ag/Bi12O17Cl2 composite: A case study of visible-light-driven plasmonic photocatalyst

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    In this investigation, novel Ag/Bi12O17C12 plasmonic composites with different Ag contents were constructed through a solvothermal and subsequent photoreduction route and fully characterized by a collection of analytical techniques. Spectroscopic results confirmed the presence and uniform dispersion of Ag nanoparticles on the 2D nanosheets of Bi12O17C12. The Ag content in composites exerted considerable influence on the extension of light-adsorption range and the enlargement of specific surface areas. The photocatalytic abilities of these Ag/Bi12O17C12 composites were evaluated toward the degradation of rhodamine B (RhB) and 2,4-dichlorophenol (2,4-DCP) under the visible-light irradiation. The results demonstrated that the Ag/Bi12O17C12 composites showed much higher photocatalytic efficiencies than that of pure Bi12O17C12, especially the sample with an optimal Ag content showing the best photocatalytic behavior among all tested samples. The remarkable enhancement of Ag/Bi12O17C12 photocatalytic efficiency could be mainly attributed to the efficient charge separation that was induced by the localized surface plasmon resonance effect of metallic Ag, strong visible-light adsorption and the favorable morphology with enlarged specific surface areas. Eventually, the photocatalysis mechanism over Ag/Bi12O17C12 composites was preliminarily proposed on the base of reactive species trapping experiments. (C) 2016 Elsevier B.V. All rights reserved

    ST-Producing E. coli Oppose Carcinogen-Induced Colorectal Tumorigenesis in Mice

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    There is a geographic inequality in the incidence of colorectal cancer, lowest in developing countries, and greatest in developed countries. This disparity suggests an environmental contribution to cancer resistance in endemic populations. Enterotoxigenic bacteria associated with diarrheal disease are prevalent in developing countries, including enterotoxigenic E. coli (ETEC) producing heat-stable enterotoxins (STs). STs are peptides that are structurally homologous to paracrine hormones that regulate the intestinal guanylyl cyclase C (GUCY2C) receptor. Beyond secretion, GUCY2C is a tumor suppressor universally silenced by loss of expression of its paracrine hormone during carcinogenesis. Thus, the geographic imbalance in colorectal cancer, in part, may reflect chronic exposure to ST-producing organisms that restore GUCY2C signaling silenced by hormone loss during transformation. Here, mice colonized for 18 weeks with control E. coli or those engineered to secrete ST exhibited normal growth, with comparable weight gain and normal stool water content, without evidence of secretory diarrhea. Enterotoxin-producing, but not control, E. coli, generated ST that activated colonic GUCY2C signaling, cyclic guanosine monophosphate (cGMP) production, and cGMP-dependent protein phosphorylation in colonized mice. Moreover, mice colonized with ST-producing E. coli exhibited a 50% reduction in carcinogen-induced colorectal tumor burden. Thus, chronic colonization with ETEC producing ST could contribute to endemic cancer resistance in developing countries, reinforcing a novel paradigm of colorectal cancer chemoprevention with oral GUCY2C-targeted agents
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