Pilot actions in European cities - Stuttgart

The field of urban climatology has a long tradition in Stuttgart. It exists as discipline in Stuttgart since 1938. Stuttgart was the first city to establish its own Department of Climatology to research ways of improving the flow of fresh air into the city and to reduce thermal stress in most populated city districts. The specialist department of Urban Climatology, within the Environmental Protection Office, deals with tasks relating to environmental meteorology within the scope of air pollution control and also relating to urban and global climate protection. So in Stuttgart the urban heat island phenomenon (UHI) is studied for several decades, leading to a high level understanding of the UHI and the problems which it causes. The UHI causes an increase in air temperatures and thermal stress, that are identified as most negative impacts on human health and urban living. In the view of global climate change and the predicted temperature rise for the Stuttgart region of 1.5–2 K in this century, the negative impacts of UHI on human health and urban living will become more problematic in the future. According to the results of climate models the frequency of very hot days is expected to jump by nearly 30 % at the end of the century. The rising temperatures due to the global climate change in combination with the temperature shift as a result of the UHI will intensify the heat stress in urban areas, that leads to a significant increasing risk to human health, in particular to the very young and elderly. Not least due its importance for the human health and the quality of urban life in Stuttgart, the UHI is focussed by urban planners and is noticed by the future development of the city. Within the pilot action study in Stuttgart several measure for reducing the UHI and the impacts on urban living and human health are analysed by the use of micro-scale and macro-scale simulations. With the help of these analysis realisable measure are selected. The most useful measures are implemented into a developmoutline plan for the redevelopment of the city district Stuttgart-West by the municipal urban planners

Plasma Magnetohydrodynamics and Energy Conversion

Contains reports on four research projects.National Science Foundation (Grant G-24073)United States Air Force, Aeronautical Systems Division, Aeronautical Accessories Laboratory, Wright-Patterson Air Force Base (Contract AF33(616)-7624

Protein phosphatase 2A promotes hepatocellular carcinogenesis in the diethylnitrosamine mouse model through inhibition of p53

Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Most HCCs develop in cirrhotic livers. Alcoholic liver disease, chronic hepatitis B and chronic hepatitis C are the most common underlying liver diseases. Hepatitis C virus (HCV)-specific mechanisms that contribute to HCC are presently unknown. Transgenic expression of HCV proteins in the mouse liver induces an overexpression of the protein phosphatase 2A catalytic subunit (PP2Ac). We have previously reported that HCV-induced PP2Ac overexpression modulates histone methylation and acetylation and inhibits DNA damage repair. In this study, we analyze tumor formation and gene expression using HCV transgenic mice that overexpress PP2Ac and liver tissues from patients with HCC. We demonstrate that PP2Ac overexpression interferes with p53-induced apoptosis. Injection of the carcinogen, diethylnitrosamine, induced significantly more and larger liver tumors in HCV transgenic mice that overexpress PP2Ac compared with control mice. In human liver biopsies from patients with HCC, PP2Ac expression was significantly higher in HCC tissue compared with non-tumorous liver tissue from the same patients. Our findings demonstrate an important role of PP2Ac overexpression in liver carcinogenesis and provide insights into the molecular pathogenesis of HCV-induced HC

Phase III study of ACVBP versus ACVBP plus rituximab for patients with localized low-risk diffuse large B-cell lymphoma (LNH03-1B)

Background The superiority of a chemotherapy with doxorubicin, cyclophosphamide, vindesine, bleomycin and prednisone (ACVBP) in comparison with cyclophosphamide, doxorubicin, vincristin and prednisone plus radiotherapy for young patients with localized diffuse large B-cell lymphoma (DLBCL) was previously demonstrated. We report the results of a trial which evaluates the role of rituximab combined with ACVBP (R-ACVBP) in these patients. Patients and methods Untreated patients younger than 66 years with stage I or II DLBCL and no adverse prognostic factors of the age-adjusted International Prognostic Index were randomly assigned to receive three cycles of ACVBP plus sequential consolidation with or without the addition of four infusions of rituximab. Results A total of 223 patients were randomly allocated to the study, 110 in the R-ACVBP group and 113 in the ACVBP group. After a median follow-up of 43 months, our 3-year estimate of event-free survival was 93% in the R-ACVBP group and 82% in the ACVBP group (P = 0.0487). Three-year estimate of progression-free survival was increased in the R-ACVBP group (95% versus 83%, P = 0.0205). Overall survival did not differ between the two groups with a 3-year estimates of 98% and 97%, respectively (P = 0.686). Conclusion In young patients with low-risk localized DLBCL, rituximab combined with three cycles of ACVBP plus consolidation is significantly superior to ACVBP plus consolidation alon

Glycemia Determines the Effect of Type 2 Diabetes Risk Genes on Insulin Secretion

OBJECTIVE—Several single nucleotide polymorphisms (SNPs) in diabetes risk genes reduce glucose- and/or incretin-induced insulin secretion. Here, we investigated interactions between glycemia and such diabetes risk polymorphisms. RESEARCH DESIGN AND METHODS—Insulin secretion was assessed by insulinogenic index and areas under the curve of C-peptide/glucose in 1,576 subjects using an oral glucose toler-ance test (OGTT). Participants were genotyped for 10 diabetes risk SNPs associated with -cell dysfunction: rs5215 (KCNJ11), rs13266634 (SLC30A8), rs7754840 (CDKAL1), rs10811661 (CDKN2A/2B), rs10830963 (MTNR1B), rs7903146 (TCF7L2), rs10010131 (WFS1), rs7923837 (HHEX), rs151290 (KCNQ1), an