Are Coyotes “Natural”? Differences in Perceptions of Coyotes Among Urban and Suburban Park Users

By 2050 more than 65% of humans are expected to live in urban and suburban areas. This shift has gained the attention of conservation scientists and managers with more focus directed on conflict and coexistence between wildlife and urbanized populations. One species that is increasingly prominent in urban and suburban environments is the coyote (Canis latrans). Coyotes have established themselves as a keystone predator with a regulating effect on prey populations, thus playing an important role in the functioning of the urban ecosystem. However, research has shown that negative perceptions of coyotes are common and contribute to support for eradication-focused management strategies, such as broad-scale trapping or culling, which are expensive and largely ineffective. To better understand coyote acceptance and non-acceptance we conducted a comparative study of park users residing in two counties in the New York metropolitan area: a suburban county, where coyotes are already established, and an urban county, where coyotes have only recently begun to arrive. Our findings suggest that urban respondents have lower levels of coyote acceptance and higher preference for coyote removal than suburban respondents. We tested multiple predictor variables to determine which was the strongest driver of desire for removal: perception of threat to humans and pets, perception of coyote “naturalness” in the environment, and appropriateness of expressed reaction to a hypothetical coyote encounter. We found that perception of coyote “naturalness” was the strongest predictor of whether people felt that coyotes belonged in the region and thus should not be removed. Our results suggest that wildlife coexistence strategies could benefit from messages that instill in residents a sense that their local area is a place where coyotes and other wild animals belong

Border Effects in House Prices

This article estimates the effect of the Dutch–German border on house prices. We argue that the difference between house prices at the border indicates the willingness to pay to stay in a country compared to living across the border. After a change in the tax rules in 2001, migration from the Netherlands to Germany increased substantially and the gradient of Dutch house price towards the German border steepened. Combining a German and Dutch real estate dataset and using different estimation strategies, we find that asking prices of comparable housing drop by about 16% when one crosses the Dutch–German border

Speculative Price Bubbles in Urban Housing Markets in Germany

The surge in the German house prices starting in 2010 raised fears about the emergence of a speculative bubble. Given a local nature of housing markets, it is not clear to what extent the bubble, if any, is spread across different cities. In this paper, we test for speculative house price bubbles in 127 large German cities over the last 20 years. Along with testing bubbles for each city separately, we apply two new testing approaches: a panel data and principal components version of explosive root tests. We define bubble as an explosive growth of prices that is not supported by the rent increase. Therefore, to check for the existence of bubbles, we examine prices, rents, and price-to-rent ratios. We find evidence for explosive price increases in many cities, especially for the case of newly built housing. However, only in few urban housing markets prices decouple from their fundamental values. On the national level, we do not see evidence for speculative price movements. Overall, we find that the danger of a build-up of a speculative price bubble in the German housing market is rather moderate

A Molecular Signature of Proteinuria in Glomerulonephritis

Proteinuria is the most important predictor of outcome in glomerulonephritis and experimental data suggest that the tubular cell response to proteinuria is an important determinant of progressive fibrosis in the kidney. However, it is unclear whether proteinuria is a marker of disease severity or has a direct effect on tubular cells in the kidneys of patients with glomerulonephritis. Accordingly we studied an in vitro model of proteinuria, and identified 231 “albumin-regulated genes” differentially expressed by primary human kidney tubular epithelial cells exposed to albumin. We translated these findings to human disease by studying mRNA levels of these genes in the tubulo-interstitial compartment of kidney biopsies from patients with IgA nephropathy using microarrays. Biopsies from patients with IgAN (n = 25) could be distinguished from those of control subjects (n = 6) based solely upon the expression of these 231 “albumin-regulated genes.” The expression of an 11-transcript subset related to the degree of proteinuria, and this 11-mRNA subset was also sufficient to distinguish biopsies of subjects with IgAN from control biopsies. We tested if these findings could be extrapolated to other proteinuric diseases beyond IgAN and found that all forms of primary glomerulonephritis (n = 33) can be distinguished from controls (n = 21) based solely on the expression levels of these 11 genes derived from our in vitro proteinuria model. Pathway analysis suggests common regulatory elements shared by these 11 transcripts. In conclusion, we have identified an albumin-regulated 11-gene signature shared between all forms of primary glomerulonephritis. Our findings support the hypothesis that albuminuria may directly promote injury in the tubulo-interstitial compartment of the kidney in patients with glomerulonephritis

Gene expression analysis in human osteoblasts exposed to dexamethasone identifies altered developmental pathways as putative drivers of osteoporosis

BACKGROUND: Osteoporosis, a disease of decreased bone mineral density represents a significant and growing burden in the western world. Aging population structure and therapeutic use of glucocorticoids have contributed in no small way to the increase in the incidence of this disease. Despite substantial investigative efforts over the last number of years the exact molecular mechanism underpinning the initiation and progression of osteoporosis remain to be elucidated. This has meant that no significant advances in therapeutic strategies have emerged, with joint replacement surgery being the mainstay of treatment. METHODS: In this study we have used an integrated genomics profiling and computational biology based strategy to identify the key osteoblast genes and gene clusters whose expression is altered in response to dexamethasone exposure. Primary human osteoblasts were exposed to dexamethasone in vitro and microarray based transcriptome profiling completed. RESULTS: These studies identified approximately 500 osteoblast genes whose expression was altered. Functional characterization of the transcriptome identified developmental networks as being reactivated with 106 development associated genes found to be differentially regulated. Pathway reconstruction revealed coordinate alteration of members of the WNT signaling pathway, including frizzled-2, frizzled-7, DKK1 and WNT5B, whose differential expression in this setting was confirmed by real time PCR. CONCLUSION: The WNT pathway is a key regulator of skeletogenesis as well as differentiation of bone cells. Reactivation of this pathway may lead to altered osteoblast activity resulting in decreased bone mineral density, the pathological hallmark of osteoporosis. The data herein lend weight to the hypothesis that alterations in developmental pathways drive the initiation and progression of osteoporosis