How Does Changing Land Cover and Land Use in New Zealand relate to Land Use Capability and Slope?

Land cover and use are critical for climate change, water quality and use, biodiversity and soil conservation as well as important drivers of rural economic activity and the evolution of rural communities. The Land Use in Rural New Zealand (LURNZ) model is a simulation model that predicts overall shifts in land use at a national scale and then allocates those changes spatially. We create a new dataset that allows us to consider fine scale land cover and use on private rural land and land characteristics associated with those land covers and uses. Second, we produce some summary statistics on the land cover transitions that were observed from 1996 to 2002. We find some evidence that supports our simple model of the relationship between land use changes and observable land quality, and the use of Land Use Capability and slope in rules to simulate the location of changes in land use and cover and also identify some directions for future work.Land use, climate change, water, soil, land use capability, LURNZ, New Zealand, spatial modelling

Urban development in coastal Oregon : discrete-choice estimation with spatial autocorrelation

Development along the Oregon coast is continuing in areas that are known to be hazardous, in spite of strict zoning and other laws. The coast commonly sees erosion that can wash away cliffs and undermine structures as well as accretion that can bury houses in sand. However the much more acute risk is the potential for a tsunami triggered by an earthquake in the ocean. This paper examines the factors influencing development along the Oregon coast using satellite imagery and other spatial data. An econometric model for land use change at the pixel level is developed. The scale at which the data (satellite imagery) are collected is different from the scale at which development occurs, leading to spatial correlation among pixels that are geographically close to each other. Estimating a standard probit model in this case leads to parameter estimates that are inconsistent. Incorporating a spatial lag of the dependent variable will account for the spatial autocorrelation but makes maximum likelihood estimation nearly impossible so a Bayesian approach is used instead. A Gibb's sampling algorithm is implemented to estimate the conditional distribution of each parameter in the model, from which parameter estimates can be derived. The Bayesian spatial probit estimation is very computationally intensive however the results indicate that the spatial lag is a crucial part of the model. This approach also allows projections of the spatial pattern of future development, unlike estimation methods that sample the data to remove autocorrelation among observations. The spatial lag model is then used to project future development patterns in several regions along the Oregon coast and explore potential applications of this projection model. In particular, predicted development patterns in the tsunami hazard zone are examined in the Waldport area, on the central coast of Oregon

Characterization of novel isoforms and evaluation of SNF2L/SMARCA1 as a candidate gene for X-linked mental retardation in 12 families linked to Xq25-26

<p>Abstract</p> <p>Background</p> <p>Mutations in genes whose products modify chromatin structure have been recognized as a cause of X-linked mental retardation (XLMR). These genes encode proteins that regulate DNA methylation (<it>MeCP2</it>), modify histones (<it>RSK2 </it>and <it>JARID1C</it>), and remodel nucleosomes through ATP hydrolysis (<it>ATRX</it>). Thus, genes encoding other chromatin modifying proteins should also be considered as disease candidate genes. In this work, we have characterized the <it>SNF2L </it>gene, encoding an ATP-dependent chromatin remodeling protein of the ISWI family, and sequenced the gene in patients from 12 XLMR families linked to Xq25-26.</p> <p>Methods</p> <p>We used an <it>in silico </it>and RT-PCR approach to fully characterize specific SNF2L isoforms. Mutation screening was performed in 12 patients from individual families with syndromic or non-syndromic XLMR. We sequenced each of the 25 exons encompassing the entire coding region, complete 5' and 3' untranslated regions, and consensus splice-sites.</p> <p>Results</p> <p>The <it>SNF2L </it>gene spans 77 kb and is encoded by 25 exons that undergo alternate splicing to generate several distinct transcripts. Specific isoforms are generated through the alternate use of exons 1 and 13, and by the use of alternate donor splice sites within exon 24. Alternate splicing within exon 24 removes a NLS sequence and alters the subcellular distribution of the SNF2L protein. We identified 3 single nucleotide polymorphisms but no mutations in our 12 patients.</p> <p>Conclusion</p> <p>Our results demonstrate that there are numerous splice variants of SNF2L that are expressed in multiple cell types and which alter subcellular localization and function. <it>SNF2L </it>mutations are not a cause of XLMR in our cohort of patients, although we cannot exclude the possibility that regulatory mutations might exist. Nonetheless, <it>SNF2L </it>remains a candidate for XLMR localized to Xq25-26, including the Shashi XLMR syndrome.</p

Characterization of novel isoforms and evaluation of SNF2L/SMARCA1 as a candidate gene for X-linked mental retardation in 12 families linked to Xq25-26

<p>Abstract</p> <p>Background</p> <p>Mutations in genes whose products modify chromatin structure have been recognized as a cause of X-linked mental retardation (XLMR). These genes encode proteins that regulate DNA methylation (<it>MeCP2</it>), modify histones (<it>RSK2 </it>and <it>JARID1C</it>), and remodel nucleosomes through ATP hydrolysis (<it>ATRX</it>). Thus, genes encoding other chromatin modifying proteins should also be considered as disease candidate genes. In this work, we have characterized the <it>SNF2L </it>gene, encoding an ATP-dependent chromatin remodeling protein of the ISWI family, and sequenced the gene in patients from 12 XLMR families linked to Xq25-26.</p> <p>Methods</p> <p>We used an <it>in silico </it>and RT-PCR approach to fully characterize specific SNF2L isoforms. Mutation screening was performed in 12 patients from individual families with syndromic or non-syndromic XLMR. We sequenced each of the 25 exons encompassing the entire coding region, complete 5' and 3' untranslated regions, and consensus splice-sites.</p> <p>Results</p> <p>The <it>SNF2L </it>gene spans 77 kb and is encoded by 25 exons that undergo alternate splicing to generate several distinct transcripts. Specific isoforms are generated through the alternate use of exons 1 and 13, and by the use of alternate donor splice sites within exon 24. Alternate splicing within exon 24 removes a NLS sequence and alters the subcellular distribution of the SNF2L protein. We identified 3 single nucleotide polymorphisms but no mutations in our 12 patients.</p> <p>Conclusion</p> <p>Our results demonstrate that there are numerous splice variants of SNF2L that are expressed in multiple cell types and which alter subcellular localization and function. <it>SNF2L </it>mutations are not a cause of XLMR in our cohort of patients, although we cannot exclude the possibility that regulatory mutations might exist. Nonetheless, <it>SNF2L </it>remains a candidate for XLMR localized to Xq25-26, including the Shashi XLMR syndrome.</p

Additional detail in aggregate integrated land-use models via simulating developer pro forma thinking

This paper describes an enhancement to MetroScope, the land-use model component of an integrated model suite used to answer current- and next-generation policy questions facing Oregon Metro (the Portland regional planning organization) and other public agencies. The enhancement is designed to simulate more-detailed housing developer decision processes within an overall aggregate spatial equilibrium model (SEM) framework via a pro forma paradigm. The paper enumerates the policy questions that motivated the enhancement, discusses the integrated model framework, briefly reviews levels of detail available in existing models as context, and frames potential future research directions for additional decision process detail that would be helpful in the consumer modules of the model and potentially other SEMs currently in use

Area Changes in U.S. Forests and Other Major Land Uses, 1982 to 2002, With Projections to 2062

This study updates an earlier assessment of the past, current, and prospective situation for the Nation’s land base. We describe area changes among major land uses on the U.S. land base for historical trends from 1982 to 2002 and projections out to 2062. Historically, 11 million acres of forest, cropland, and open space were converted to urban and other developed uses from 1992 to 1997 on nonfederal land in the contiguous United States. The national rate of urbanization increased notably compared to the 1982-92 period. The largest percentage increase was in urban use, which grew by 10 percent or 7.3 million acres between 1997 and 2001. Forest land was the largest source of land converted to developed uses such as urbanization. Urban and other developed areas are projected to continue to grow substantially, in line with a projected U.S. population increase of more than 120 million people over the next 50 years, with population growth the fastest in the West and South. Projected increases in population and income will, in turn, increase demands for use of land for residential, urban, transportation, and related uses. Area of nonfederal forest-land cover in the United States is projected to decline over the next half-century, with a 7-percent reduction by 2062. Projected increases in urban and developed uses will likely intensify competition for remaining land between the agricultural and forestry sectors. Reversions to forest land have generally been from grassland used as pasture. All three major land use classes—cropland, forest land, and grassland—have lost area to urbanization, and that trend is projected to continue