Application of a grid-scale lateral discharge model in the BALTEX region

In this study, a hydrological discharge model is presented which may be applied as a tool to validate the simulation of the hydrologic cycle of atmospheric models that are used in climate change studies. It can also be applied in studies of global climate change to investigate how changes in climate may affect the discharge of large rivers. The model was developed for the application with the climate models used at the Max-Planck- Institute for Meteorology. It describes the translation and retention of the lateral waterflows on the global scale as a function of the spatially distributed land surface characteristics which are globally available. Here, global scale refers to the resolution of 0.5° and lower, corresponding to a typical average gridbox area of about 2500 km2. The hydrological discharge model separates between the flow processes of overland flow, baseflow and overflow. The model parameters are mainly functions of the gridbox characteristics of topography and gridbox length. The hydrological discharge model is applied to the BALTEX (Baltic Sea Experiment) region using input from an atmospheric general circulation model (ECHAM4) as well as from a regional climate model (REMO). The simulated inflows into the Baltic Sea and its sub- catchments are compared to observed and naturalized discharges. The results of this comparison are discussed and the simulated values of precipitation, surface air temperature and accumulated snowpack are compared to both observed data and surrogate data

Responses of an experimental solid tumour to irradiation: A comparison of modes of fractionation.

Several radiotherapeutic schedules compatible with continued structural-functional integrity of the gastrointestinal (GI) mucosa were compared utilizing the P815X2 murine mastocytoma grown as a solid subcutaneous tumour. Both the tumour and underlying normal tissues were irradiated during the treatments. The tumour exhibited a Do that increased from 210 rad to 397 rad as the tumour aged and in all instances demonstrated minimal shoulders in survival curves. In spite of a relative radioresistance of cells within the solid tumour, quite effective control of localized disease could be accomplished with radiotherapy schemes compatible with GI tolerance limits. Schedules evaluated utilizing this model included acute exposures to 1122 rad, daily exposure to 187 rad, 5 days/week exposures to 281 rad, twice weekly exposures (561 rad on Mondays and 374 rad on Thursdays) and a high dose, two fractions per day, schedule. Tumours were followed for changes in growth patterns during these schedules. Efficacy of tumour control was determined and schedules were compared on this basis. Aggressive radiotherapy approaching the tolerance limits of any of the fractionation schemes proved most effective

Underground bio-methanation: Concept and potential

As a major part of the energy turn around, the European Union and other countries are supporting the development of renewable energy technologies to decrease nuclear and fossil energy production. Therefore, efficient use of renewable energy resources is one challenge, as they are influenced by environmental conditions and hence, the intensity of resources such as wind or solar power fluctuates. To secure constant energy supply, suitable energy storage and conversion techniques are required. An upcoming solution is the utilization and storage of hydrogen or hydrogen-rich natural gas in porous formations in the underground. In the past, microbial methanation was observed as a side effect during these gas storage operations. The concept of underground bio-methanation arised, which uses the microbial metabolism to convert hydrogen and carbon dioxide into methane. The concept consists of injecting gaseous hydrogen and carbon dioxide into an underground structure during energy production peaks which are subsequently partly converted into methane. The resulting methane-rich gas mixture is withdrawn during high energy demand. The concept is comparable to engineered bio-reactors which are already locally integrated into the gas infrastructure. In both technologies, the conversion process of hydrogen into methane is driven by hydrogenotrophic methanogenic archaea present in the aqueous phase of the natural underground or above-ground engineered reactor. Nevertheless, the porous medium in the underground provides, compared to the engineered bio-reactors, a larger interface between the gas and aqueous phase caused by the enormous volume in the underground porous media. The following article summarizes the potential and concept of underground methanation and the current state of the art in terms of laboratory investigations and pilot tests. A short system potential analysis shows that an underground bio-reactor with a storage capacity of 850 Mio. Sm could deliver methane to more than 600,000 households, based on a hydrogen production from renewable energies

Genetic Ablation of Nrf2/Antioxidant Response Pathway in Alexander Disease Mice Reduces Hippocampal Gliosis but Does Not Impact Survival

In Alexander disease (AxD) the presence of mutant glial fibrillary acidic protein (GFAP), the major intermediate filament of astrocytes, triggers protein aggregation, with marked induction of a stress response mediated by the transcription factor, Nrf2. To clarify the role of Nrf2 in AxD, we have crossed Gfap mutant and transgenic mouse models into an Nrf2 null background. Deletion of Nrf2 eliminates the phase II stress response normally present in mouse models of AxD, but causes no change in body weight or lifespan, even in a severe lethal model. AxD astrocytes without Nrf2 retain features of reactivity, such as expression of the endothelin-B receptor, but have lower Gfap levels, a decrease in p62 protein and reduced iron accumulation, particularly in hippocampus. Microglial activation, indicated by Iba1 expression, is also diminished. Although the Nrf2 response is generally considered beneficial, these results show that in the context of AxD, loss of the antioxidant pathway has no obvious negative effects, while actually decreasing Gfap accumulation and pathology. Given the attention Nrf2 is receiving as a potential therapeutic target in AxD and other neurodegenerative diseases, it will be interesting to see whether induction of Nrf2, beyond the endogenous response, is beneficial or not in these same models

Deletion within the Src homology domain 3 of Bruton's tyrosine kinase resulting in X-linked agammaglobulinemia (XLA).

The gene responsible for X-linked agammaglobulinemia (XLA) has been recently identified to code for a cytoplasmic tyrosine kinase (Bruton's agammaglobulinemia tyrosine kinase, BTK), required for normal B cell development. BTK, like many other cytoplasmic tyrosine kinases, contains Src homology domains (SH2 and SH3), and catalytic kinase domain. SH3 domains are important for the targeting of signaling molecules to specific subcellular locations. We have identified a family with XLA whose affected members have a point mutation (g-->a) at the 5' splice site of intron 8, resulting in the skipping of coding exon 8 and loss of 21 amino acids forming the COOH-terminal portion of the BTK SH3 domain. The study of three generations within this kinship, using restriction fragment length polymorphism and DNA analysis, allowed identification of the mutant X chromosome responsible for XLA and the carrier status in this family. BTK mRNA was present in normal amounts in Epstein-Barr virus-induced B lymphoblastoid cell lines established from affected family members. Although the SH3 deletion did not alter BTK protein stability and kinase activity of the truncated BTK protein was normal, the affected patients nevertheless have a severe B cell defect characteristic for XLA. The mutant protein was modeled using the normal BTK SH3 domain. The deletion results in loss of two COOH-terminal beta strands containing several residues critical for the formation of the putative SH3 ligand-binding pocket. We predict that, as a result, one or more crucial SH3 binding proteins fail to interact with BTK, interrupting the cytoplasmic signal transduction process required for B cell differentiation