Climate Change and Restoration of Degraded Land

The United Nations Climate Change Conference, Durban 2011, delivered a breakthrough on the international community's response to climate change. In the second largest meeting of its kind, the negotiations advanced, in a balanced fashion, the implementation of the Convention and the Kyoto Protocol, the Bali Action Plan, and the Cancun Agreements. The outcomes included a decision by Parties to adopt a universal legal agreement on climate change as soon as possible, and no later than 2015. One of the decisions adopted by COP 17 and CMP 7 regard to the land use, land-use change and forestry, and invites the Intergovernmental Panel on Climate Change to review and, if necessary, update supplementary methodologies for estimating anthropogenic greenhouse gas emissions by sources and removals by sinks resulting from land use, land-use change and forestry activities under Article 3, paragraphs 3 and 4, of the Kyoto Protocol. Land degradation is a human-induced or natural process which negatively affects the productivity of land within an ecosystem. The direct causes of land degradation are geographically specific. Climate change, including changes in short-term variation, as well as long-term gradual changes in temperature and precipitation, is expected to be an additional stress on rates of land degradation. Book Topics: • Introduction to Climate Change and Land Degradation • Change Mitigation • Climate Change and Waste Land Restoration • Water Management and Planning • Erosion and Hydrological Restoration • Forest Fire Land Restoration • Polluted Soils Restoration • Combating Climate Change by Restoration of Degraded Land • Research Matters – Climate Change Governance • Advanced Statistics Climate Change and Restoration of Degraded Land is of interests to academics, engineers, consultans, designers and professionals involved in restoration of degraded lands projects.

Evaluación de un forward modelling de ondas sísmicas : aplicación práctica del efecto source ghost

Se ha utilizado un programa de modelización de ondas sísmicas por métodos finitos en dos dimensiones para analizar el efecto Source Ghost en profundidades de 4, 14, 24 y 34 metros. Este efecto se produce cuando se dispara una fuente enterrada y, debido al contacto suelo-aire, se genera una onda reflejada que, en cierto momento, se superpone con la onda principal, produciéndose una disminución de la amplitud de la onda (Source Ghost). Los resultados teóricos del efecto se han comparado con los resultados prácticos del programa de modelización concluyéndose que es posible determinar el rango de frecuencias afectado por el efecto. Sin embargo, la distancia entre receptor y fuente es una nueva variable que desplaza el efecto hacia frecuencias más altas impidiendo su predicción. La utilización de una técnica de procesamiento básica como la corrección del Normal Move-Out (NMO) en el apilado de las trazas, contrarresta la variable distancia receptor-fuente, y por tanto es posible calcular el rango de frecuencias del efecto Source Ghost. Abstract A seismic wave forward modeling in two dimensions using finite-difference method has been used for analyzing the Source Ghost effect at depths between 4-34 meters. A shot from a buried source generates a down going reflection due to the free surface boundary and, at some point, it interferes with the main wave propagation causing a reduction of wave amplitude at some frequency range (Source Ghost). Theoretical results and experimental results provided by the forward modeling are compared for concluding that the forward modeling is able to identify the frequency range affected by the source ghost. Nevertheless, it has been found that the receiver-source distance (offset) is a new variable that modifies the frequency range to make it unpredictable. A basic seismic processing technique, Normal Move-Out (NMO) correction, has been used for a single twenty fold CMP gather. The final stack shows that the processing technique neutralize the offset effect and therefore the forward modeling is still capable to determine the affected frequency range by the source ghost regardless the distance between receiver and source.

Identification of an ATP-binding cassette transporter involved in bicarbonate uptake in the cyanobacterium Synechococcus sp. strain PCC 7942

Exposure of cells of cyanobacteria (blue–green algae) grown under high-CO2 conditions to inorganic C-limitation induces transcription of particular genes and expression of high-affinity CO2 and HCO3− transport systems. Among the low-CO2-inducible transcription units of Synechococcus sp. strain PCC 7942 is the cmpABCD operon, encoding an ATP-binding cassette transporter similar to the nitrate/nitrite transporter of the same cyanobacterium. A nitrogen-regulated promoter was used to selectively induce expression of the cmpABCD genes by growth of transgenic cells on nitrate under high CO2 conditions. Measurements of the initial rate of HCO3− uptake after onset of light, and of the steady-state rate of HCO3− uptake in the light, showed that the controlled induction of the cmp genes resulted in selective expression of high-affinity HCO3− transport activity. The forced expression of cmpABCD did not significantly increase the CO2 uptake capabilities of the cells. These findings demonstrated that the cmpABCD genes encode a high-affinity HCO3− transporter. A deletion mutant of cmpAB (M42) retained low CO2-inducible activity of HCO3− transport, indicating the occurrence of HCO3− transporter(s) distinct from the one encoded by cmpABCD. HCO3− uptake by low-CO2-induced M42 cells showed lower affinity for external HCO3− than for wild-type cells under the same conditions, showing that the HCO3− transporter encoded by cmpABCD has the highest affinity for HCO3− among the HCO3− transporters present in the cyanobacterium. This appears to be the first unambiguous identification and description of a primary active HCO3− transporter.

Assembly of a Novel Cartilage Matrix Protein Filamentous Network: Molecular Basis of Differential Requirement of von Willebrand Factor A Domains

Cartilage matrix protein (CMP) is the prototype of the newly discovered matrilin family, all of which contain von Willebrand factor A domains. Although the function of matrilins remain unclear, we have shown that, in primary chondrocyte cultures, CMP (matrilin-1) forms a filamentous network, which is made up of two types of filaments, a collagen-dependent one and a collagen-independent one. In this study, we demonstrate that the collagen-independent CMP filaments are enriched in pericellular compartments, extending directly from chondrocyte membranes. Their morphology can be distinguished from that of collagen filaments by immunogold electron microscopy, and mimicked by that of self-assembled purified CMP. The assembly of CMP filaments can occur from transfection of a wild-type CMP transgene alone in skin fibroblasts, which do not produce endogenous CMP. Conversely, assembly of endogenous CMP filaments by chondrocytes can be inhibited specifically by dominant negative CMP transgenes. The two A domains within CMP serve essential but different functions during network formation. Deletion of the A2 domain converts the trimeric CMP into a mixture of monomers, dimers, and trimers, whereas deletion of the A1 domain does not affect the trimeric configuration. This suggests that the A2 domain modulates multimerization of CMP. Absence of either A domain from CMP abolishes its ability to form collagen-independent filaments. In particular, Asp22 in A1 and Asp255 in A2 are essential; double point mutation of these residues disrupts CMP network formation. These residues are part of the metal ion–dependent adhesion sites, thus a metal ion–dependent adhesion site–mediated adhesion mechanism may be applicable to matrilin assembly. Taken together, our data suggest that CMP is a bridging molecule that connects matrix components in cartilage to form an integrated matrix network.