Designing sustainable and economically attractive brownfield revitalization options using an integrated assessment model.

We describe the development of an integrated assessment model which evaluates redevelopment options of large contaminated brownfields and we present the application of the model in a case study. Aiming to support efficient and sustainable revitalization and communication between stakeholders, the presented assessment model integrates three pinnacles of brownfield revitalization: (i) subsurface remediation and site preparation costs, (ii) market-oriented economic appraisal, and (iii) the expected contribution of planned future land use to sustainable community and regional development. For the assessment, focus is set on the early stage of the brownfield redevelopment process, which is characterized by limited data availability and by flexibility in land use planning and development scope. At this stage, revealing the consequences of adjustments and alterations in planning options can foster efficiency in communication between the involved parties and thereby facilitates the brownfield revitalization process. Results from the case-study application indicate that the integrated assessment provides help in the identification of land use options beneficial in both a sustainable and an economical sense. For the study site it is shown on one hand that brownfield redevelopment is not automatically in line with sustainable regional development, and on the other hand it is demonstrated that additional contributions to sustainability are not intrinsically tied to increased costs.

Overexpressed vs mutated Kras in murine fibroblasts: a molecular phenotyping study.

Ras acts in signalling pathways regulating the activity of multiple cellular functions including cell proliferation, differentiation, and apoptosis. Amino-acid exchanges at position 12, 13, or 61 of the Kras gene convert the proto-oncogene into an activated oncogene. Until now, a direct comparison of genome-wide expression profiling studies of Kras overexpression and different Kras mutant forms in a single assay system has not been carried out. In our study, we focused on the direct comparison of global gene expression effects caused by mutations in codon 12 or 13 of the Kras gene and Kras overexpression in murine fibroblasts. We determined Kras cellular mRNA, Ras protein and activated Ras protein levels. Further, we compared our data to the proteome analysis of the same transfected cell lines. Both overexpression and mutations of Kras lead to common altered gene expression patterns. Only two genes, Lox and Col1a1, were reversely regulated in the Kras transfectants. They may contribute to the higher aggressiveness of the Kras codon 12 mutation in tumour progression. The functional annotation of differentially expressed genes revealed a high frequency of proteins involved in tumour growth and angiogenesis. These data further support the important role of these genes in tumour-associated angiogenesis.

Proteinuria and immunoglobulinuria in neonatal dogs.

Samples of urine and serum from 45 newborn rottweiler puppies from six litters, and milk from their mothers, were taken 24, 48 and 72 hours and seven and 14 days after birth. Urine total protein and creatinine concentrations were determined and the ratios calculated. The immunoglobulin (Ig) concentrations of IgG, IgM and IgA in urine, serum and milk were determined with a commercially available elisa kit. The concentration of total protein in urine decreased from 1.64 to 0.29 mg/ml, and it and the ratio of total protein to creatinine in the urine of the neonatal puppies exceeded the normal values for adult dogs, but all the puppies developed normally. The average concentration of IgG in urine decreased from 0.0035 to 0.0003 mg/ml, that of IgA from 0.0035 to 0.0002 mg/ml and that of IgM from 0.0006 mg/ml to undetectable levels after two weeks. After two weeks, 47 per cent of the puppies had measurable levels of IgA and 70.6 per cent had measurable levels of IgG, but none of them had measurable levels of IgM.