Competing redox reactions in Fe-containing AlO(OH) and Al2O 3 matrices: A combined investigation by Mössbauer, ESR spectroscopy and thermal analysis

The investigation of iron-doped AlO(OH)/Al2O3 systems revealed that the combined employment of Mössbauer and ESR spectroscopies together with thermal analysis yields meaningful data with complementary information. This mutual complementarity is based on the coexistence of Fe point defects with the corresponding aggregated FeOx species which has been observed even for very low Fe concentrations. Competing redox processes between the dopant, the AlOx matrix, and the gas atmosphere during the thermal treatment enable the generation of solid phases exhibiting specific chemical properties. The entire reaction process is influenced by a specific mechanical and thermal pre-treatment that affects predominantly oxydative processes in the matrix. A protecting influence of the matrix preventing further reductive attack of the Fe3+ Fe2+ ions by hydrogen has been established

Molecular switching in iron complexes bridged via tin-cyanides observed by Mössbauer and ESR spectroscopy

The precursor [FeIII(L)Cl] (LH2 N,N'-bis(2'-hydroxy- 3'-X-benzyliden)-1,6-diamino-3-N-hexane) is a high-spin (S 5/2) complex (with X -CH3, -O-CH3). This precursor is combined with the bridging unit [SnIV(CN)4] to yield star-shaped pentanuclear clusters, [(L-X-FeIII)4Sn(CN) 4]Cl4 57Fe-Mössbauer, 119mSn- Mössbauer, and ESR spectroscopy are used to study our samples. For X -CH3 the 57Fe-Mössbauer data show a multiple spin transition between iron(III) in the high-spin and low-spin state. Changing the functional group from X -CH3 to X -O-CH3 turns the switchability off

The microwave cavity perturbation technique for contact-free and in situ electrical conductivity measurements in catalysis and materials science

We have developed a noncontact method to probe the electrical conductivity and complex permittivity of single and polycrystalline samples in a flow-through reactor in the temperature range of 20–500 °C and in various gas atmospheres. The method is based on the microwave cavity perturbation technique and allows the simultaneous measurement of microwave conductivity, permittivity and of the catalytic performance of heterogeneous catalysts without any need for contacting the sample with electrodes. The sensitivity of the method towards changes in bulk properties was proven by the investigation of characteristic first-order phase transitions of the ionic conductor rubidium nitrate in the temperature range between 20 and 320 °C, and by studying the temperature dependence of the complex permittivity and conductivity of a niobium(V)-doped vanadium-phosphorous-oxide catalyst for the selective oxidation of n-butane to maleic anhydride. Simultaneously, the catalytic performance was probed by on line GC analysis of evolving product gases making the technique a real in situ method enabling the noninvasive investigation of electronic structure–function relationships

Mathematical modeling reveals threshold mechanism in CD95-induced apoptosis

Mathematical modeling is required for understanding the complex behavior of large signal transduction networks. Previous attempts to model signal transduction pathways were often limited to small systems or based on qualitative data only. Here, we developed a mathematical modeling framework for understanding the complex signaling behavior of CD95(APO-1/Fas)-mediated apoptosis. Defects in the regulation of apoptosis result in serious diseases such as cancer, autoimmunity, and neurodegeneration. During the last decade many of the molecular mechanisms of apoptosis signaling have been examined and elucidated. A systemic understanding of apoptosis is, however, still missing. To address the complexity of apoptotic signaling we subdivided this system into subsystems of different information qualities. A new approach for sensitivity analysis within the mathematical model was key for the identification of critical system parameters and two essential system properties: modularity and robustness. Our model describes the regulation of apoptosis on a systems level and resolves the important question of a threshold mechanism for the regulation of apoptosis